Immuno PPT Flashcards Unit 3
What is autoimmune diseases?
What is the cause of autoimmune
diseases?
What is central tolerance?
How is autoimmunity maintained in the
secondary lymphoid organs?
Which one is implicated as primary
mediators of autoimmune disease?
Why is Th1 cells primary mediators of
autoimmune disease?
Which one react to foreign antigens?
What makes an individual more
susceptible to a particular autoimmune
disease?
What other several mechanisms are
thought be contribute to autoimmunity?
What is the example of antigens that are
protected from encountering the
circulation are not exposed to potentially
reactive lymphocytes?
What is the Molecular mimicry refers?
What is the last major factor?
What is the one B-cell defect in
particular?
How these defects may enhanced?
What are some other defects of the
immune system?
Which hormone play a role?
What affect estrogens?
How autoimmune disease classified?
What is Systemic lupus erythematosus?
Who is more likely to these disease?
There is an interplay between ________
Autoimmune diseases is a conditions in which
damage to organs or tissues results from the presence
of autoantibody or autoreactive cells.
The loss or breakdown of self-tolerance brought by
several mechanism, including clonal deletion of
relevant effector cells and active regulation by T cell.
It is the destruction of potentially self-reactive
lymphocytes.
By a delicate balance between the T helper cell type
1(Th1) and T helper cell type 2(Th20 populations.
Th1 cell.
Because they release pro-inflammatory cytokines.
Th2 response.
The inheritance of jean coding for a specific major
histocompatibility complex (MHC).
The release of sequestered antigens, molecular
mimicry, and polyclonal B-cell activation.
Sperm.
It refers the fact that many individual viral or
bacterial agents contain antigens that closely
resemble self-antigens.
Polyclonal B-cell activation.
Fc receptor polymorphisms.
By organisms such as gram negative bacteria and
several viruses, including cytomegalovirus and
Epstein-Barr-virus.
The influence of hormones, and environmental
conditions.
Estrogens.
They are known to affect cytokine production and
may influence with T cells, either Th1 or Th2, are
more active in a particular response.
As systemic or organ specific.
It is a chronic systemic inflammatory disease marked
by alternating exacerbations and remissions.
Women are much more likely than men, by a margin
of 10 to 1.
Genetic susceptibility and environmental.
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Immuno PPT Flashcards Unit 3
and _________ factor in the
development of the disease.
Which play a role in presentation of
HLA antigens.
foreign or self- antigen to T cells and B
cells?
What abnormalities have also been found Fcy receptors on B cells, macrophages, dendritic
in SLE?
cells, and neutrophils that bind IgG and prevent
excess immune reactions.
Is environmental factors important?
Yes it is include exposure to ultraviolet light, certain
medications, and infectious agents.
Is hormones are also important factor?
Yes, because they may influence the regulation of
genes for SLE expression.
What are the clinical signs of SLE?
It is extremely diverse, and nonspecific symptoms
such as fatigue, weight loss, malaise, fever, and
anorexia are often the first appear.
What are another symptoms of SLE?
Joint involvement, skin manifestations, a classic
butter fly rash across the nose and cheeks may
develop.
What exhibit evidence seen in one-half
The exhibit evidence of renal involvement, with
to two-thirds of all patients?
diffuse proliferative glomerulonephritis, being the
most dangerous.
What other conditions are develop?
It develop include deposition of immune complexes
in the sub endothelial tissues and thickening of the
basement membranes.
_____is the most frequent cause of death Renal failure.
in patients with SLE.
What other systemic effects may
Cardiac involvement with pericarditis, tachycardia,
include?
or ventricular enlargement, pruritus with chest pains,
neuropsychiatric manifestations such as seizures,
mild cognitive dysfunction, psychosis or depression,
or hematologic abnormalities such as anemia or
lymphopenia.
What was the first clue in the mystery of The discovery of the LE-cell by Malcolm Hargraves
lupus?
in 1948.
What was the next discovery?
SLE, is associated with more than 25 autoantibodies.
Auto reactivity of T and B cell leading
The production of autoantibodies.
to_______.
What is one of the main immunologic
The constant presence of antigenic material that
characteristics in lupus?
triggers polyclonal activation of B cells
What results from accompanying
An enhanced production of certain cytokins that
alteration in the function of both Th1 contribute to up regulation of antibody production by
and Th2 helper cells?
B cells.
What does IL-10 trigger?
An increase in antibodies directed against DNA.
What does IL-10 stimulate to
Platelet activating factor
produce.
When immune complexes are
Because of the other possible immune system
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Immuno PPT Flashcards Unit 3
formed, why can’t they be cleared as
usual from the circulation?
Why is accumulation of IgG to
double stranded DNA seem to be the
most pathogenic.
How does drug induced lupus differ
from the more chronic form of the
disease?
What are the most common drugs
used for drug induced lupus
What is the first test performed when
SLE is suspected
Why is fluorescent antinuclear
antibody (FANA) testing used the
most.
FANA is a sensitive test and easy to
use but has low diagnostic
specificity, why?
What is the percentage that yield
false positive results on the FANA
test.
What is the percent of SLE patients
that yield false negative results
What is the common practice to
screen to avoid low positive titers in
the normal population
On FANA what does SLE patients
show under the microscope
Why are dsDNA antibodies most
specific for SLE
What does antibodies to ds-DNA
typically produce on FANA testing
What other assays can be used to
detect antibodies to ds-DNA
Why is EIA most widely used
technique
What is the second major antibody
found in lupus patients
What is histone
What do histones do
What can be detected in almost all
patients with drug induced lupus
What supports the diagnosis of drug
disruptions.
It forms complexes of an intermediate size that
become deposited in the glomerular basement
membrane of the kidney nephron which activates
complement cascade and causes kidney damage.
Symptoms usually disappear once the drug is
discontinued
Anticonvulsants and oral contraceptives
Screening test for antinuclear antibodies (ANA)
It detects a wide range of antibodies and is positive in
about 95% of patients with SLE.
Many of the antibodies are associated with other
autoimmune diseases
2% of healthy individuals and up to 75% of older
individuals
5%
1:80 dilution or 1:160 if the patient is over 65
Either a homogeneous pattern representing
fluorescence of the entire nucleus or staining of the
periphery of the nucleus occurs.
They are mainly seen in patients with lupus and
levels correlate with disease activity
Peripheral or a homogeneous staining pattern
Immunodiffusiom, RIA, EIA
Because its considered more sensitive
antihistone antibody
A nucleoprotein that is a major constituent of
chromatin
They wrap the DNA like a spool of thread
antihistone antibody
Presence of antihistone antibody alone or combined
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Immuno PPT Flashcards Unit 3
induced lupus
Where else is antihistone antibodies
found
What does high levels of antihistone
antibodies tend to be associated with
How are antihistone antibodies
typically detected
What is it when antibodies stimulated
by DNA complexed to histone
known as
How did anti-SM antibody get its
name
Why is anti-Sm antibody specific for
SLE
What kind of pattern does FANA
testing show under a microscope
What is used in simple slide
agglutination test for SLE
What also belongs to the family of
extractable nuclear antigens
Another method that ANAs can be
detected is by
What does Immunodiffusion method
typically used for
What does ouchterlony double
diffusion detect and what does a
positive reaction indicate
EIA is also used to detect
What are the benefits of EIA testing
How does immunoblotting
techniques separate out antigens
What is used to visualize individual
bands during immunoblotting
techniques
What are Antiphospholipid
antibodies
What does Antiphospholipid
antibodies affect
with antibody to ss-DNA
Inrheumatoid arthritis and primary biliary cirrhosis
The more active and severe forms of SLE
by immunofluorescent assays, immunoblotting, EIA
Deoxyribonucleoprotein
Antibody to a preparation of extractable nuclear
antigen was first described in a patient named smith
Because its not found in other autoimmune diseases
A coarsely speckled pattern of nuclear fluorescence
Latex particles coated with DNP
SS-A/Ro and SS-B/LA antigens
Immunodiffusion
To determine the immunologic specificity of a
positive FANA test
Detects antibody to several of the small nuclear
ribonucleoproteins or extractable nuclear antigens
(ENA), and is indicated by immunoprecipitation
lines of serological identity
Anti-ds-DNA, antihistone antibodies, anti-SS-A, and
anti-SS-B
Testing is quantitative, is less subjective and lends
itself well to automation
By means of polyacrylamide gel electrophoresis
followed by blotting to a nitrocellulose sheet, and
incubation with dilutions of patient serum, r
Radiolabeled or enzyme antibody conjugates
A heterogeneous group of antibodies that bind to
phospholipid alone or are complexed with protein
Affects every organ in the body, but they are
especially associated with deep-vein and arterial
thrombosis and with morbidity in pregnancy
How was the lupus anticoagulant,
Because it produced prolonged activated partial
which was one of the several types of thromboplastin time (aPTT) and prothrombin time
antiphospholipid antibodies, named? (PT)
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Immuno PPT Flashcards Unit 3
What disease does the lupus
anticoagulant can cause false positive
results on.
What risks do patients with lupus
anticoagulant antibody have
Another example of a systemic
autoimmune disorder is
What is the population that
rheumatoid arthritis affects
What ages does rheumatoid arthritis
occur
How can rheumatoid arthritis be
characterized
What is the progression of
rheumatoid arthritis
What is the strongest association of
RA with certain MHC class II genes?
What are the key symptoms of
Rheumatoid Arthritis?
What are the clinical signs of
rheumatoid arthritis?
About 20% of patients have nodules
over the bones. Where can nodules
also be found?
What are the other systemic
symptoms of RA?
What are the symptons of Felty’s
Syndrome?
What are the proinflammatory
cytokines found in synovial fluid?
How much percent of patients with
RA have the rheumatoid factor
antibody?
Where does complement protein C1
Syphilis
An increased risk of clotting and spontaneous
abortion, and platelet function may be affected
Rheumatoid arthritis
1% population, women are three times as likely to be
affected then men
Between ages 35 and 50 but can occur at any age
A chronic, symmetric, and erosive arthritis of the
peripheral joints that can also affect multiple organs
such as the heart and the lungs, and a decline in
functional ability and reduced life expectancy
It varies, because there may be spontaneous
remissions or an increasingly active disease in some
individuals that rapidly progresses to joint deformity
and disability
DR4 alleles
Morning stiffness around the joints lasting at least 1
hour; swelling of the soft tissue around three or more
joints; swelling of the proximal interphalangeal,
metacarpophalangeal, or wrist joints; symmetric
arthritis; subcutaneous nodules; a positive test for
rheumatoid factor; and radiographic evidence of
erosions in the joints of the hands, the wrists, or both
Malaise, fatigue, fever, weight loss, and transient
joint pain that begins in the small joints of the hands
and feet.
Myocardium, pericardium, heart valves, pleura,
lungs, spleen, and larynx.
Anemia, formation of subcutaneous nodules,
perdicarditis, lymphadenopathy, splenomegaly,
interstitial lung disease, or vasculitis
Chronic RA coupled with neutropenia,
splenomegaly, and thrombocytopenia
Interleukin-1, interleukin-6, interleukin-8,
interleukin-15, interleukin-18 and tumor necrosis
factor-alpha
75 percent
Immune complexes
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Immuno PPT Flashcards Unit 3
binds to that activates the classical
complement cascade?
What is the lead marker for detection
of RA?
What is classically most often tested
for to aid in making the initial
diagnosis?
What are the two types of
agglutination tests for RF?
Will the negative result for
agglutination test rule out the
presence of RA?
What other diseases can RF be found
in?
How much percentage of RFnegative patients are positive for
anti-CCP?
What are the laboratory findings for
the diagnosis of RA?
What are the traditional therapy for
RA?
What does rituximab specifically
targets on B cells?
In the disease Hashimoto’s
thyroiditis, the follicles with the
thyroid are filled with material which
is called?
What is thyroglobulin?
How does the TRH acts on the
pituitary?
Genes associated with a
predisposition to thyroid
autoimmunity can be divided into 2
groups: What are the 2 groups?
What does immune-modulating
genes include?
What does thyroid-specific genes
include?
What is another name for
Anti-CCP
RF antibody
One is using sheep RBCs coated with IgG and the
other is using latex particles coated with the same
antigen.
No
Syphilis, SLE, chronic active hepatitis, tuberculosis,
leprosy, infectious mononucleosis, malaria, and
Sjorgren’s syndrome.
Approximately 35-40 percent
CRP and ESR are elevated, and the level of
complement components is normal or increased,
indication increased synthesis.
Anti-inflammatory drugs such as salicylates and
ibuprofen to control local swelling and pain
CD 20 antigen
Colloid
It is the primary constituent of colloid, a large
iodinated glycoprotein, which is the precursor of the
thyroid hormones triiodothyronine (T3) and
thyroxine (T4)
Induce release of TSH
Immune-modulating genes and thyroid-specific
genes.
HLA antigens, cytotoxic T lymphocyte associated
factor-4 (CTLA-4), and protein tyrosine phosphatase22 (PTPN22)
the thyroglobulin gene and the thyroid-stimulating
hormone receptor (TSHR) genes
Under-secreting thyroid or chronic autoimmune
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Immuno PPT Flashcards Unit 3
Hashimoto’s thyroiditis?
What does Hashimoto’s thyroiditis
patients develop?
What are the symptoms of
hypothyroidism?
What is Graves’ disease
characterized by?
What are the disease manifestations
of Graves’ disease?
What are the major antibodies found
in Graves’ disease?
Does a negative test result for
antithyroglobulin antibody test rule
out Hashimoto’s disease?
What is the treatment for
Hashimoto’s disease?
What is the chronic autoimmune
disease that occurs in genetically
susceptible individuals as a result of
environmental factors?
How do you characterize
Autoimmune diabetes mellitus?
What does progressive inflammation
of the islets of Langerhans leads to?
What disease is an inflammatory
autoimmune disorder of the central
nervous system?
How are multiple sclerosis
characterized?
What are the 2 most common tests
for diagnosis of MS?
What is an autoimmune disease that
affects the neuromuscular junction?
What are the symptoms of
myasthenia gravis?
thyroiditis
Patients develop a combination of goiter (or enlarged
thyroid), hypothyroidism, and thyroid autoantibodies.
dry skin, decreased sweating, puffy face with
edematous eyelids, pallor with a yellow tinge, weight
gain, and dry and brittle hair.
Hyperthyroidism
thyrotoxicosis, with an enlarged goiter, accompanied
by nervousness, insomnia, depression, weight loss,
heat intolerance, sweating, rapid heartbeat,
palpitations, breathlessness, fatigue, cardiac
dysrhythmias, and restlessness
thyroid-stimulating hormone receptor antibody
(TSHRab) and antibodies to thyroid peroxidase
No
Thyroid hormone replacement therapy, Monitoring
the TSH levels, surgery to remove part of the thyroid
gland
Autoimmune diabetes mellitus, of IA diabetes
insufficient insulin production caused by selective
destruction of the beta cells of the pancreas, located
in clusters called the islets of Langerhans
Fibrosis and destruction of most beta cells
Multiple Sclerosis
the formation of lesions called plaques in the white
matter of the brain and spinal cord, resulting in the
progressive destruction of the myelin sheath of axons
Oligoclonal banding and the CSF IgG index
Myasthenia gravis. It is characterized by weakness
and fatigability of skeletal muscles
Early signs are drooping of the eyelids and the
inability to retract the corners of the mouth, often
resulting in a snarling appearance. Other symptoms
may include difficulty in speaking, chewing, and
swallowing and inability to maintain support of the
trunk, the neck, or the head. If respiratory muscle
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Immuno PPT Flashcards Unit 3
What is RIA?
What is Goodpasture’s syndrome?
What are the symptoms of
Goodpasture’s syndrome?
What is Addison’s disease?
What disease can Addison’s disease
progress to?
What is scleroderma?
What is pernicious anemia?
What vitamin cannot be absorbed
when you have pernicious anemia?
When does autoimmune hemolytic
anemia occurs?
What is Idiopathic
Thrombocytopenic Purpura?
What is purpura?
What are lymphoid malignancies
weakness occurs, it can be life threatening. Onset of
symptoms can be acute, resembling a stroke, or they
may develop slowly and worsen over time.
RIA is used to detect antibody, based on assays that
block the binding of receptors by anti-ACH receptor
(ACHR) antibody. A radio-labeled snake venom
called α-bungarotoxin is used to irreversibly bind to
ACHRs. Precipitation of receptors caused by
combination with antibody is then measured.
characterized by the presence of autoantibody to
glomerular, renal tubular, and alveolar basement
membranes That can rapidly progressed to renal
failure.
Signs of renal involvement include gross or
microscopic hematuria, proteinuria, decreased
creatinine clearance, and increased BUN and
creatinine levels. Pulmonary symptoms include
hemorrhage, dyspnea, weakness, fatigue, and cough.
When the adrenal glands do not produce sufficient
steroid hormones. Characterized by a low blood
glucose, low blood pressure, and hyperpigmentation
in the gums and nail beds.
Addisonian crisis.
Also known as systemic sclerosis, a chronic systemic
autoimmune disease characterized by hardening of
the skin.
Loss of gastric parietal cells, which are responsible
for the secretion of intrinsic factor, a protein essential
for subsequent absorption of vitamin B12 in the
ileum
Vitamin B12
When antibodies directed against the person’s own
RBCs cause them to burst, leading to insufficient
plasma concentration
Isolated low platelet count with normal bone marrow
and the absence of other causes of thrombocytopenia.
It causes a characteristic purpuric rash and an
increased tendency to bleed.
red or purple discolorations on the skin that do not
blanch on applying pressure. They are caused by
bleeding underneath the skin usually secondary to
vasculitis from autoimmune distruction or dietary
deficiency of vitamin C (scurvy).
Leukemias and lymphomas
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Immuno PPT Flashcards Unit 3
classified as?
Differentiate leukemia and
lymphoma.
What does plasma cell dyscrasias
primarily include?
What does immunoproliferative
diseases commonly involve?
What is the term for an excess
accumulation of cells?
True or false?: Malignancies are
generally due to one factor in onset.
List two ways in which malignancies
occur
What is apoptosis?
Why cells of the immune system are
at great risk for malignant
transformation?
The lymphomas are divided into
what two categories?
The Rappaport classification is
determined solely on what?
The Working Formulation
Classification Scheme, which
ultimately became the standard, was
based on what?
How did the Working Formulation
Classification Scheme classify
lymphomas?
1994, the International Lymphoma
Study Group proposed what
classification scheme?
What is Revised European-American
Lymphoma (REAL) Classification?
How does the REAL scheme divide
NHL?
In leukemias, malignant cells are primarily present
in the bone marrow and peripheral blood. In
lymphomas, the malignant cells arise in lymphoid
tissues, such as lymph nodes, tonsils, or spleen.
Multiple myeloma and Waldenstrom’s
macroglobulinemia
Bone marrow, lymphoid organs and other
nonlymphoid sites.
Malignancy
False: Malignancies are generally multifactorial in
onset.
1. Rapid proliferation of cells
Normal proliferation of cells that fail to undergo
apoptosis
2. Programmed cell death
3. The features that characterize the
development of malignancy are also a normal
part of the immune response – an antigenic
stimulus results in proliferation of lymphoid
cells and a high rate of mutation during gene
rearrangement and affinity maturation
4. Hodgkin’s lymphoma (HL) and nonHodgkin’s lymphoma (NHL)
5. Morphological features by light microscopy
6. Lymph node architecture and cytology of
malignant cells as seen by light microscopy
7. Low-, intermediate-, and high-grade
processes, based on the aggressiveness of the
untreated lymphoma
8. Revised European-American Lymphoma
(REAL) Classification
9. A list that set forth the diagnostic features of
lymphomas that the group members
considered to be widely recognized and
clearly diagnosable by contemporary
techniques, including immunologic,
cytogenetic, and molecular techniques.
10. Into neoplasms of precursor cells and
neoplasms of mature cells of B, T, or natural
killer (NK) cell lineage
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Immuno PPT Flashcards Unit 3
What classification scheme is the
basis for the one adopted by the
WHO?
What immunoproliferative disease is
a highly treatable and often curable
lymphoma that occurs both in young
adults and older adults?
Hodgkin’s Lymphoma (HL) is
characterized by the presence of what
cells and where?
Describe Reed-Sternberg (RS) cells
True or False: Reed-Sternberg (RS)
cells may be in the B-Cell Lineage
True or False: Epidemiological
studies suggest that HL has an
infectious etiology.
In order to reflect the differences in
clinical presentation, morphology,
phenotype, and molecular features,
the REAL/WHO classification
recognizes a basic distinction
between what two types of HL?
Patients with HL have elevated levels
of what?
What is the causative agent of
infectious mononucleosis?
What is the most sensitive method to
detect presence of latent EBV
infections in RS cells?
NHL includes a wide range of
neoplasms. What % are B-cell
lymphomas in the U.S.?
True or False: NHL lymphomas tend
to be slowly progressive and
compatible with long-term survival,
while others are typically highly
aggressive and rapidly fatal if not
treated
Which is more difficult to
characterize? T-cell or B-cell
lymphomas?
Why are T-cell lymphomas more
difficult to characterize than B-cell
lymphoma?
11. REAL scheme
12. Hodgkin’s Lymphoma (HL)
13. Reed-Sternberg (RS) cells in affected lymph
nodes and lymphoid organs
14. Typically large with a bilobed nucleus and 2
prominent nucleoli
15. True
16. True
17. Nodular lymphocyte predominant HL (NLPHL) and classic HL
18. Antibody to Epstein-Barr Virus (EBV)
19. EBV
20. RNA assay for EBV-encoded RNAs: EBER1
and EBER2
21. 85% of NHL cases are B-cell lymphomas
22. True
23. T-cell lymphomas
24. B-cell lymphomas can be tested for
monotypic light-chain expression; whereas no
easy way exists to assay the clonality in a
similar way with T-cell lymphomas. Also,
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Immuno PPT Flashcards Unit 3
True or False: Some T-cell
syndromes progress stealthily form
atypical but non-clonal proliferations
into clonal malignancies.
What are the 2 general categories of
leukemia?
What type of leukemia is usually
slowly progressive and compatible
with extended survival?
What type of leukemia is generally
much more rapidly progressive but
has a higher response rate to therapy
compared to the chronic leukemias.
This leukemia is characterized by
presence of very poorly differentiated
precursor cells (blast cells) in the
bone marrow and peripheral blood
Immunologically, ALL is divided
into how many types?
What are the 4 types of ALL?
What type of leukemia is a group of
diseases almost exclusively of B-cell
origin.
Chronic lymphocytic leukemia
(CLL), small lymphocytic lymphoma
(SLL), prolymphocytic leukemia
(PL), and hairy cell leukemia (HCL)
are examples of what type of
leukemia?
The World Health Organization
(WHO) considers these leukemias a
single disease with different clinical
presentations.
This leukemia is a common
hematopoietic malignancy that
involves the expansion of a clone of
B cells that have the appearance of
small mature lymphocytes.
This leukemia is a rare, slowly
progressive disease characterized by
infiltration of the bone marrow and
some T-cell syndromes progress stealthily
form atypical but non-clnoal proliferations
into clonal malignancies.
25. True
Acute or Chronic
26.
Chronic leukemia
Acute leukemia
Acute lymphoblastic leukemia (ALL)
4
CALLa (CD10)-expressing immature B cell ALL,
pre-B cell ALL without CALLa, T-cell ALL, and Bcell ALL.
Chronic lymphocytic leukemias/lymphomas
Chronic lymphocytic leukemias/lymphomas
Chronic lymphocytic leukemia (CLL)/small
lymphocytic lymphoma (SLL),
Chronic lymphocytic leukemia (CLL)
Hairy cell leukemia
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Immuno PPT Flashcards Unit 3
spleen by leukemic cells, without
involvement of lymph nodes.
In Hairy cell leukemias, patients
usually present with cytopenias
because of ____.
True or False: In Hairy cell leukemia,
the blood lymphocyte count is not
very high usually.
Describe appearance of malignant
lymphocytes in HCL
Plasma cell dyscrasias include
several related syndromes. What are
they?
Plasma cell dyscrasias are
characterized by the overproduction
of what?
True or False: M protein is usually
associated with other
lymphoproliferative disorders, such
as non-Hodgkin lymphoma (NHL) or
primary amyloidosis.
True or False: Laboratory evaluation
is not important in the diagnosis and
differentiation of plasma cell
dyscrasias conditions.
Diagnosis and monitoring of the
plasma cell dyscrasias depend
heavily on detecting and quantifying
what protein?
What disease is a malignancy of
mature plasma cells that accounts for
about 10 percent of all hematologic
cancers?
Which is the most serious and most
common of the plasma cell
dyscrasias?
Patients progress from the
asymptomatic ___ to ___ to the
symptomatic disease of multiple
myeloma.
Patients with multiple myeloma
typically have excess plasma cells in
Bone marrow infiltration
True
Round with a “bland” cytological appearance. They
often have irregular, “hairy” cytoplasmic projections
from their cytoplasmic surfaces.
multiple myeloma, Waldenström’s
macroglobulinemia, and the premalignant conditions
monoclonal gammopathy of undetermined
significance (MGUS) and smoldering multiple
myeloma (SMM)
A single immunoglobulin component called a
myeloma protein (M protein), or paraprotein, by a
clone of plasma cells.
False. It is rarely associated with these.
False
M protein
Multiple myeloma
Multiple myeloma
monoclonal gammopathy of undetermined
significance (MGUS); smoldering multiple myeloma
(SMM).
bone marrow; bone lesions
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Immuno PPT Flashcards Unit 3
____ a monoclonal immunoglobulin
component in the plasma and/or
urine, and lytic
_____.
True or False: In multiple myeloma
plasma cells infiltrating the bone
marrow may be morphologically
normal or may show atypical or
bizarre cytological features.
In multiple myeloma, the
immunoglobulin produced by the
malignant clone can be of any type.
Which is the most common?
In multiple myeloma, the
immunoglobulin produced by the
malignant clone can be of any type.
After IgG, which 2 are the most
common?
Why are an excess of free light
chains produced in multiple
myeloma?
In what percent of cases do myeloma
cells exclusively produce light
chains?
Free light chains are rapidly excreted
in ___.
What are free immunoglobulin light
chains (κ or λ) excreted in the urine?
True or False: In multiple myeloma,
very rarely, two or more distinct M
proteins are produced, or a clinically
typical myeloma may produce no
secretory product
In multiple myeloma, compare the
level of normal immunoglobulin to
the amount of M protein present in
the serum
The clinical manifestations of
multiple myeloma are primarily ___,
___ and ___.
What percent of patients with
multiple myeloma develop light-
True
IgG (50%)
IgA and IgM (light chains only)
Very often the production of heavy and light chains
by the malignant plasma cells are not well
synchronized
10%
Urine
Bence Jones protein
True
The level of normal immunoglobulin is often
decreased in proportion to the amount of M protein
present in the serum
Hematologic, skeletal, and immunologic.
15%
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Immuno PPT Flashcards Unit 3
chain deposition disease or
amyloidosis
What two related disorders have free
light chains or fragments of
immunoglobulin deposited in the
tissues?
How do amyloid fibers stained with
the dye Congo red appear when
viewed under a polarizing
microscope?
Deposits of light chains in multiple
myeloma can be identified in what
specimens? With what techniques?
Criteria for the diagnosis of multiple
myeloma include?
M proteins can be detected in serum
or urine by what 2 methods?
An important feature supporting the
diagnosis of multiple myeloma is the
presence of this protein in urine
Free light chains can be detected in
serum or urine by what 2 methods?
What disease is a malignant
proliferation of IgM-producing
lymphocytes and corresponds to
lymphoplasmacytoid lymphoma as
defined by the WHO?
Describe the malignant cells of
Waldenström’s macroglobulinemia
The clinical signs and symptoms of
Waldenström’s macroglobulinemia
are?
The following symptoms are
indicative of what
immunoproliferative disease?
Weakness, fatigue, anemia, bleeding,
and hyperviscosity
How common are lytic bone lesions,
hypercalcemia, and renal tubular
abnormalities in Waldenström’s
macroglobulinemia?
light-chain deposition disease and amyloidosis
Apple-green birefringence
Tissue sections; immunofluorescence or
immunohistochemical staining with specific
antibodies.
plasma cells constituting greater than 10 percent of
bone marrow cells or a plasmacytoma (a solid tumor
mass of plasma cells), plus either serum M protein
greater than 3g/dL, urinary M protein, or osteolytic
bone lesions.
electrophoresis and immunofixation
Bence Jones protein
electrophoresis and immunofixation
Waldenström’s macroglobulinemia
Malignant cells are more immature than plasma cells
and have a microscopic appearance somewhere
between that of small lymphocytes and plasma cells.
Infiltration of the malignant cells into bone marrow,
the spleen, and lymph nodes with the overproduction
of monoclonal IgM
Waldenström’s macroglobulinemia
They are rare
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Immuno PPT Flashcards Unit 3
All individuals with Waldenström’s
macroglobulinemia have elevated
serum monoclonal protein that
migrates in the ___ region.
True or False: In WM, the
concentration of the monoclonal IgM
varies widely, and it is not possible
to define a concentration that
differentiates this disease from other
B-cell lymphoproliferative disorders
In 10–20 percent of WM patients, the
IgM paraproteins behave as ___.
Cryoglobulins precipitate at what
temperature?
What type of proteins can occlude
small vessels in the extremities in
cold weather in WM?
In WM, some IgM paraproteins have
specificity for i or I antigens and will
agglutinate red blood cells in the
cold; they are referred to as ____.
Approximately 20 percent of patients
with Waldenström’s
macroglobulinemia will present with
what symptom?
The laboratory is involved in how
many major ways in evaluating
lymphoproliferative disorders?
The lab assesses the
immunophenotype of hematopoetic
cells in the bone marrow or lymphoid
tissues using what technique?
True or False? One of the major roles
of the lab is to evaluate the amount
and characteristics of
immunoglobulins.
An assessment of of genetic and
chromosomal abnormalities in
hematopoietic malignancies is not
assessed by the laboratory.
In the diagnosis and classification of
leukemias and lymphomas, flow
cytometry is used to analyze cell
surface marker ___ antigen
expression
What lab technique is ideal for fluids
Gamma
True
Cryoglobulins
Cold temperatures;
Cryoglobulins
cold agglutinins
peripheral neuropathy
3
Flow cytometry
True
False
CD (cluster of differentiation)
Flow cytometry
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Immuno PPT Flashcards Unit 3
in which cells are naturally
suspended, but it is also useful in
lymphoid tissues, from which singlecell suspensions can be easily made
What lab technique can
simultaneously analyze, even in
small samples, multiple-cell
properties, including size,
granularity, and surface and
intracellular antigen.
What is monoclonal gammopathy?
The evaluation of a patient for the
possibility of a monoclonal
gammopathy requires both
qualitative and quantitative analysis
of what?
The initial tests used to screen for the
presence of a monoclonal
gammopathy are?
True or False? Quantitative
measurement of serum or urine
immunoglobulins is used in the
diagnosis of some
lymphoproliferative disorders
What is the name of the technique in
which serum proteins are separated
on the basis of their size and
electrical charge
Additional evaluation of serum
immunoglobulin is performed if the
SPE shows a ___ component; if there
is a significant quantitative
abnormality of serum
immunoglobulins, or if the clnical
picture strongly suggests a plasma
cell ____.
Myeloma in which only light chains
are produced may not be detected
using what technique and why?
After SPE, what 2 techniques that
may be used in the next step in
evaluating a monoclonal
gammopathy?
Compare immunoelectrophoresis
Flow cytometry
In a malignant disorder, the clonal proliferation of
transformed plasma cells leads to overproduction of a
single immunoglobulin
Immunoglobulins
serum immunoglobulin levels and serum protein
electrophoresis
True
Serum protein electrophoresis (SPE)
Monoclonal; dyscrasia
Serum protein electrophoresis (SPE), because the
light chains are rapidly cleared in the urine.
immunoelectrophoresis (IEP) or immunofixation
electrophoresis (IFE).
IFE is much faster than IEP, has much greater
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Immuno PPT Flashcards Unit 3
(IEP) and immunofixation
electrophoresis (IFE) in terms of
accuracy and sensitivity.
On immunofixation, areas of diffuse
staining indicate______, while
monoclonal bands produce narrow,
intensely stained bands
The majority of B-cell lymphomas
and some T-cell lymphomas are
characterized by specific
chromosome _____.
Specific chromosome translocations
are of particular value in diagnosis of
disease such as many B-cell and Tcell lymphomas. These can usually
be detected using:
List two common secondary
chromosome events (secondary to
specific chromosome translocations)
that are rarely specific to particular
type of lymphoma but provide
valuable prognostic information
Traditional cytogenetic evaluation
has been expanded by a technique
known as?
True or False: Lymphoid
malignancies can also be evaluated
by molecular genetic techniques.
What methods are usually geared
toward finding clonal rearrangements
of the immunoglobulin gene in B-cell
malignancies or of the T-cell receptor
gene in T-cell malignancies.
What type of rearrangements are too
subtle to be detected by conventional
cytogenetics and must use FISH or
molecular genetic techniques?
What technique allows the efficient
measurement of expression for
almost every gene in the human
genome in a single overnight
hybridization experiment.
What genomic-scale approach has
begun to reveal novel molecularbased subclasses of many
malignancies, including lymphoma
sensitivity, and is the most accurate assay for typing
paraproteins.
polyclonal immunoglobulins
Translocations
Cytogenic techniques
Aneuploidy (abnormal number of chromosomes) and
deletion of specific chromosome regions
fluorescence in situ hybridization (FISH)
True
fluorescence in situ hybridization (FISH) and
molecular genetic techniques.
Clonal rearrangements of the immunoglobulin gene
in B-cell malignancies or of the T-cell receptor gene
in T-cell malignancies.
complementary DNA (cDNA) microarray technology
complementary DNA (cDNA) microarray technology
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Immuno PPT Flashcards Unit 3
and leukemia?
What organ system is a diverse and
complicated network of many
biochemical and cellular
components?
Primary immunodeficiency
syndromes are rare, with the
exception of ___ deficiency.
True or False: a defect in one arm of
the immune system may affect other
aspects of immune function as well
The components of the humoral and
cell-mediated portions of the immune
system interact extensively through
many ___.
A deficiency of one component of
the system is often accompanied by
_____of other component, including
allergic or autoimmune
manifestations
Over how many different congenital
forms of immunodeficiency have
been reported, including defects in
lymphoid cells, phagocytic cells, and
complement proteins?
True or False: The clinical symptoms
associated with immune deficiencies
range from very mild or subclinical
to severe recurrent infections or
failure to thrive.
In general, defects in humoral
immunity result in pyogenic bacterial
infections, particularly where?
Defects in T-cell-mediated immunity
result in recurrent infections with
what type of intracellular pathogens?
What system is part of the innate,
antigen-nonspecific immune
response and includes neutrophils
and mononuclear phagocytic cells.
What system is activated to produce
biologically active molecules that
enhance inflammation and promote
lysis of cells and microorganisms.
What are the mechanisms of the
agammaglobulinemias?
Immune system
IgA
True
Regulatory and effector loops
hyperactivity
120
True
upper and lower respiratory tract.
viruses, fungi, and intracellular bacteria
The phagocytic system
The complement system
Genetic defects in B-cell maturation or mutations
leading to defective interactions between B and T
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Immuno PPT Flashcards Unit 3
In evaluating immunoglobulin
deficiency states, it is important to
remember this varies with age
When does IgM reach normal adult
levels?
When does IgG reach normal adult
levels?
True or False: In some normal
children, IgA levels do not reach
normal adult values until
adolescence.
All infants experience low levels of
immunoglobulins at approximately
____ of age, but in some cases, the
low levels persist for a longer time.
Transient hypogammaglobulinemia
of infancy (THI) may result due to
what?
What is the mechanism of transient
hypogammaglobulinemia?
In THI, what type of immunity is
normal?
In THI, what Ig is the most affected,
dropping at least 2 SDs below the
age-adjusted mean?
THI patients have normal numbers of
circulating CD19 positive B-cells
unlike what agammaglobulinemia?
First described in 1952, this
agammaglobulinemia is X
chromosome–linked, and so affects
males almost exclusively.
Patients with X-linked
agammaglobulinemia lack what type
of circulating cell?
Patients with X-linked
agammaglobulinemia lack
immunoglobulins of what class?
Patients with Bruton’s
agammaglobulinemia have no
plasma cells in their lymphoid
tissues, but do have this type of cell
in their bone marrow?
What type of lymphocytes are found
in normal numbers and function in
cells.
blood levels of immunoglobulins
1st year of age
5-6 years of age
True.
5-6 months
Low levels of immunoglobulins past 5-6 months of
age
Unknown
Cell-mediated immunity
IgG
Bruton’s agammaglobulinemia
Bruton’s agammaglobulinemia
Mature CD19 positive B-cell
All classes
pre-B cells
T cells
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Immuno PPT Flashcards Unit 3
Patients with Bruton’s
agammaglobulinemia?
What type of recurring infections do
these patients develop beginning in
infancy, as maternal antibody is
cleared.
What results from arrested
differentiation at the pre-B cell stage,
leading to a complete absence of B
cells and plasma cells.
What is the underlying genetic
mechanism in X-linked
hypogammaglobulinemia?
What enzyme is the apparent cause
of failure of Vh gene rearrangement?
Agammaglobulinemia can be
differentiated from transient
hypogammaglobulinemia of infancy
by the absence of what?
Are most patients with IgA
deficiency symptomatic or
asymptomatic?
Those patients with symptoms
usually have infections of the
respiratory and gastrointestinal tract
and an increased tendency to what
types of autoimmune diseases?
What other disorders are more
common among these patients.
Although the genetic defect has not
been established, it is hypothesized
that the IgA deficiency is caused by
what?
What group of disorders is common
variable immunodeficiency (CVI)?
This disorder is considered a lowincidence disorder; although it still
remains the most common primary
immune deficiency with a severe
clinical syndrome.
How is the CVI disorder acquired?
Is it seen more in men or women?
What is CVI characterized by?
What can it lead to?
recurrent bacterial infections
X-linked hypogammaglobulinemia
It is a deficiency of an enzyme called the Bruton
tyrosine kinase (Btk) in B-cell progenitor cells.
Lack of the Btk enzyme
CD19 positive B cells in the peripheral blood, by the
abnormal histology of lymphoid tissues, and by its
persistence beyond 2 years of age.
asymptomatic
Systemic lupus erythematosus, rheumatoid arthritis,
celiac disease, and thyroiditis.
Allergic disorders and malignancy
Impaired differentiation of lymphocytes to become
IgA-producing plasma cells.
It falls under the heterogeneous group of disorders.
The common variable immunodeficiency syndrome.
Congenital or acquired, familial or sporadic.
It occurs with equal frequency in men and women.
Hypogammaglobulinemia
Recurrent bacterial infections, particularly sinusitis
and pneumonia.
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Immuno PPT Flashcards Unit 3
What percentage of CVI patients
develop herpes zoster (shingles)?
What immunoglobulin is usually
deficient?
What type of reoccurring infections
are typically seen when diagnosing
patients that demonstrate a low
serum IgG level?
In contrast to X-linked
agammaglobulinemia, most patients
with CVI have normal numbers what
type of cell?
How many subclasses of IgG are in
humans?
Out of the IgG, what percentage of
the IgG1 is normally present?
Out of the IgG, what percentage of
the IgG2 is normally present?
Out of the IgG, what percentage of
the IgG3 is normally present?
Out of the IgG, what percentage of
the IgG4 is normally present?
In patients with recurrent infections,
what other testing should be
performed if the total IgG levels are
normal but the clinical picture
suggests immunoglobulin deficiency.
If the total IgG level was normal
could there still be a deficiency in
one of the subclasses?
Increased bacterial infections may
result from what?
Defects in cell-mediated immunity
can result from abnormalities in what
stages?
What types of defects can result in
severe combined immunodeficiency
(SCID)?
Besides primary defects in cellmediated immunity what other
effects can happen?
In general, defects in cellular
immunity are more difficult to
manage than what other defects?
Patients with severe defects in cellmediated immunity may develop
20 percent, which is a much higher incidence than in
immunologically normal young adults.
Both IgA and IgG, but selective IgG deficiency may
occur.
They tend to have recurrent bacterial infections.
Mature B cells
Four
About 70 percent
About 20 percent
About 6 percent
About 4 percent
levels of the different subclasses should be measured.
Yes, a deficiency of a single IgG subclass may not
result in a total IgG level below the normal range.
IgG subclass deficiencies.
Many different stages of T-Cell development
Molecular defects
Can also have secondary effects on humoral
immunity.
Defects in humoral immunity
They can develop graft-versus-host (GvH) disease.
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Immuno PPT Flashcards Unit 3
what disease?
This happens when the donor
lymphocytes are allowed to survive,
proliferate, and attack the recipient’s
tissue as foreign.
When can GvH disease occur?
GvH disease also occurs in patients who
have received this type of transplant.
This anomaly affects thymic
development.
All organs derived from these structures
can be affected.
DiGeorge anomaly associated
abnormalities include what?
•
The severity and extent of the
developmental defect can be quite
variable in this disease.
The immunodeficiency associated
DiGeorge anomaly is a quantitative
defect in what type of cells?
Insufficient types of these are made, but
those that are present are functionally
normal.
One immunodeficiency state for which a
specific enzymatic basis has been
defined is what?
The condition presents in what age group
and has recurrent or chronic pulmonary
infections, oral or cutaneous candidiasis,
diarrhea, skin infections, urinary tract
infections, and failure to thrive.
An enzyme involved in the metabolism
of purines is what affects this deficiency.
What causes the number of T cells to
progressively decrease because of the
accumulation of this toxic purine
metabolite?
This can be caused by a defect that
affects development of both types of
lymphocytes or a defective interaction
between the two limbs of the immune
system.
A severe defect in the T-cell system.
GvH disease can occur in any individual with a
severe defect in cell-mediated immunity (e.g., in
bone marrow transplant recipients) and can be fatal.
A bone marrow transplant.
DiGeorge anomaly is a developmental abnormality
of the third and fourth pharyngeal pouches that
affects thymic development.
Embryonic structures
Mental retardation, absence of ossification of the
hyoid bone, cardiac anomalies, abnormal facial
development, and thymic hypoplasia.
DiGeorge anomaly
Thymocytes
Mature T cells
Purine nucleoside phosphorylase (PNP) deficiency, a
rare autosomal recessive trait.
The condition presents in infancy
PNP- Purine nucleoside phosphorylase
Deoxyguanosine triphosphate
Defects in both humoral (B cell) and cell-mediated
(T cell) immunity
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Immuno PPT Flashcards Unit 3
a) What are the combined deficiencies are
referred to?
b) The most serious of the congenital
immune deficiencies is this?
c) SCID is actually a group of related
diseases that all affect what?
d) What is the most common form of the
SCID disease?
e) The abnormal gene involves codes for a
protein chain called the common gamma
chain, which is common to these Il
receptors.
f) What chromosome is the gene that is
referred to as the IL2RG gene located?
g) Normal signaling cannot occur in cells
with defective receptors, thus halting
what?
h) This gene is required for processing an
interleukin binding signal from the cell
membrane to the nucleus.
i) Depending on the presence of any
additional defect in the JAK3 gene, may
result is these phenotypes?
j) In such cases, no antibody production or
lymphocyte proliferative response
follows this.
k) Caused of SCID can also be identified as
what type of defects?
l) Patients with this immune deficiency
generally present early in infancy with
infection by nearly any type of organism,
including oral candidal infections,
pneumonia, and diarrhea.
m) This is a rare is a rare X-linked recessive
syndrome.
n) It is defined by the triad of what?
o) WAS is usually lethal in childhood
because of?
p) Abnormalities exist in both the cellular
and humoral arms of the immune system,
related to a general defect in what?
q) This manifests as a severe deficiency of
the naturally occurring antibodies to
what antigens?
using a shorthand of T+-B+-NK+-, with the
superscript +- denoting whether each cell type is
deficient.
Severe combined immunodeficiency (SCID).
T- and B-cell function but with differing causes
X-linked SCID
Interleukins 2, 4, 7, 9, 15, and 21.
X chromosome
natural maturation
The JAK3 gene
Either a T-B+NK+ or a T-B+NK- phenotype
An antigen or mitogen challenge.
Other molecular defects
SCID Severe combined immunodeficiency
Wiskott-Aldrich syndrome (WAS)
Immunodeficiency, eczema, and thrombocytopenia.
Infection, hemorrhage, or malignancy.
Antigen processing
Blood group antigens (isohemagglutinins).
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Immuno PPT Flashcards Unit 3
r) In addition, these patients have
persistently increased levels of what?
s) What is the primary molecular defect in
the syndrome?
t) Abnormalities cause defective in what?
u) It also affects its signal transduction in
what?
v) The laboratory features of WAS include
what?
w) This is a rare autosomal recessive
syndrome characterized by cerebellar
ataxia and telangiectasias, especially on
the earlobes and conjunctiva.
x) Blood vessels in the sclera of the eyes
may be dilated, and there may also be
this characteristic rash on part of the
face.
y) What disease do 95 percent of patients’
exhibit increased levels of serum alphafetoprotein?
z) Abnormal genes produce a combined
defect in this type of immunity.
aa) Antibody response to antigens,
especially to this, is blunted.
bb) What levels immunoglobulin’s are often
low or absent, although the pattern can
be quite variable?
cc) In addition, the number of circulating
what type of cells is often decreased.
dd) This is a group of disorders inherited as
either an X-linked or autosomal
recessive gene that affects neutrophil
microbicidal function.
ee) This disease accounts for 70 percent of
the cases, and it tends to be more severe.
ff) Symptoms of CGD include recurrent
what?
Serum alpha-fetoprotein.
It appears to be an abnormality of the integral
membrane protein CD43, which is involved in the
regulation of protein glycosylation.
Actin polymerization
Lymphocytes and platelets
A decrease in platelet number and size, prolonged
bleeding time, and bone marrow changes with a
normal or somewhat increased number of
megakaryocytes
Ataxia-telangiectasia (AT)
Reddish butterfly area on the face and ears.
WAS or Ataxia-telangiectasia (AT)
Check book
Both humoral and cellular immunity
polysaccharides
IgG2, IgA, and IgE
T cells
Chronic granulomatous disease (CGD)
X-linked disease
Suppurative infections, pneumonia, osteomyelitis,
draining adenopathy, liver abscesses, dermatitis, and
hypergammaglobulinemia.
The neutrophil abnormalities
gg) CGD is the most common and best
characterized of this type of
abnormalities?
hh) There are three different autosomal
Nicotinamide adenine dinucleotide phosphate
recessive genes involved, and all of these (NADPH) oxidase.
24
Immuno PPT Flashcards Unit 3
affect subunits of what?
ii) What normally leads to the production of
reactive oxygen molecules, such as
hydrogen peroxide (H2O2), by NADPH
oxidase on the plasma membrane?
jj) These granules fuse with, and release
their contents into, the forming
phagosome, as organisms are
phagocytized.
kk) What is used by the granule enzyme
myeloperoxidase to generate the potent
microbicidal agent hypochlorous acid.
ll) The process of generating partially
reduced forms of oxygen by stimulated
neutrophils was first detected as what?
mm)
This response was originally
termed the neutrophil “respiratory
burst”; a more correct term is called?
• In CGD, neutrophils are unable to do
what?
nn)
• CGD was historically diagnosed by
measuring the ability of a patient’s
neutrophils to reduce what dye?
1.
• More recently, this assay has become
available.
1.
1.
In this assay, what are
neutrophils labeled with?
• DHR will do what when it is reduced.
2.
1.
The neutrophils are then
activated using this, which is
mitogenic for neutrophils.
2.
The resultant oxidative burst will
reduce the DHR, resulting in
what?
• Neutrophils from CGD patients will be
unable to undergo this reaction and will
show less fluorescence than normal
neutrophils.
3.
1.
This deficiency leads to an
inability to generate enough
NADPH to supply reducing
Normally, neutrophil stimulation
Neutrophil granules
Hydrogen peroxide
An increase in oxygen consumption.
“oxidative burst.”
undergo the oxidative burst
The dye nitro-blue tetrazolium (NBT)
a flow cytometric assay
dihydrorhodamine (DHR)
fluoresce
Phorbol myristate acetate (PMA)
Fluorescence that may be quantified by flow
cytometry.
oxidative burst
Neutrophil glucose-6-phosphate dehydrogenase
deficiency.
25
Immuno PPT Flashcards Unit 3
•
•
•
•
•
equivalents to the NADPH
oxidase system.
2.
This deficiency leads to a defect
in hydrogen peroxide production
and a clinical picture similar to
that of what other disease?
Even if this is normal, neutrophils cannot
perform their functions properly if they
fail to leave the vasculature and migrate
to a site of incipient infection.
3.
These play important roles in
microbicidal activity.
1.
What causes a protein deficiency in a
component of adhesion receptors on
neutrophils, monocytes, and T cells?
What proteins does LAD affect in
neutrophils, monocytes, and T cells?
•
How are the leukocytes affected with
LAD?
What is the clinical manifestation with
LAD?
•
How can a CD18 defect be diagnosed?
•
What can lead to deficiencies in each of
the major complement components and
lead to various clinical sequelae?
Deficiencies in early complement
components (C1q, C4 and C2) are
associated with what type of syndrome?
Which is the most common complement
component deficiency?
What differentiates C3 deficiency from
other lupus-like clinical presentation?
What infection is associated with
deficiencies in the later components of
complement (C5-C9)?
Measurement of the levels of
are
used to screen for defects in antibody
production.
What is easily performed by the
transfusion service?
An overall assessment of the antibody-
•
•
•
•
•
•
•
CGD (Chronic granulomatous disease)
microbicidal activity
Adhesion receptors on leukocytes and their counterreceptors on endothelial cells and extracellular matrix
LAD: Leukocyte adhesion deficiency
Neutrophils: CD18
Monocytes: CD11b or CD11c
T cells: CD11a
Abnormal adhesion, motility, aggregation,
chemotaxis, and endocytosis
Delayed wound healing, chronic skin infections,
intestinal and respiratory tract infections, and
periodontitis
By detecting a decreased amount of CD11/18 antigen
with flow cytometry.
LAD: Leukocyte adhesion deficiency
Lupus-like syndrome
A deficiency in C2
And increased likeliness of recurrent encapsulated
organism infection.
Neisseria meningitidis
Serum IgG, IgM, IgA, and levels of the subclasses of
IgG
Assay for isohemagglutinins
Antibody response to antigens that the population is
26
Immuno PPT Flashcards Unit 3
•
•
mediated immunity can be made by
measuring:
Delayed-hypersensitivity- type skin
reactions can be used to screen for
defects in:
True or False:
Immunodeficiency Disease test are
generally performed by laboratory
personnel.
Screening for complement deficiencies
begins with?
CH50 assay can determine?
A flow cytometric assay can detect what
defect in neutrophil activity?
When is more specialized testing
probably be necessary to precisely
identify an immune abnormality?
Flow cytometry can also enumerate
in
the peripheral blood, bone marrow, and
lymph nodes.
An absence or profound decrease in the
number of CD3 positive cell is consistent
with:
When CD19 positive B cells are absent it
suggest?
True or False:
Genetic testing is available for many
immunodeficiency conditions.
By assessing the ability of isolated T
cells to proliferate in response to an
antigenic stimulus or to nonspecific
mitogens in culture, what can be
measured?
An increase in
uptake suggest cell
division and activation.
What can be measured without the use of
radioactive materials?
As of August 2008, three assays to
measure antigen- or mitogen-stimulated
T-cell activation for diagnostic use was
cleared by which federal entity?
What is the measured in a workup of
both immunodeficiency states and some
lymphoproliferative disorders?
What is used to make the quantitative
measurements of serum and urine
exposed normally or following vaccination.
Cell-mediated immunity
False: The screenings are done by the clinician.
CH50 assay
The level of functional complement in an individual.
Defect in neutrophil oxidative burst activity
1. The screening tests detect an abnormality.
2. The clinical suspicion is high.
Classes of lymphocytes
DiGeorge Syndrome
Bruton’s agammaglobulinemia
True
T-cell function.
Thymidine
Antigen- or mitogen-stimulated T-cell activation
FDA
Quantitative measurements of serum and urine
immunoglobulins.
Protein electrophoresis
27
Immuno PPT Flashcards Unit 3
immuoglobulins?
What method allows for reproducible
separation of the major plasma proteins>
What determines if additional evaluation
of the serum is necessary?
Immunofixation electrophoresis (IFE) is
another method to characterize:
When does immunofixation
electrophoresis result in areas of diffuse
staining?
What produces narrow, intensely stained
bands in IFE?
What does IFE with a lack of bands
indicate in immunodeficiencies?
How can specific immunoglobulin
isotype levels be determined?
How are monoclonal gammopathies or
immunodeficiencies evaluated?
What is the transfer of tissue from one
area of the body to another of the same
individual the graft is called?
What is the graft called when there is
transfer of cells or tissues between
identical twins?
Where is an allograft tissue/cell
transferred?
Where is a xenograft tissue/cell
transferred?
Why is transplantation utilized?
In 2006, how many solid organ
transplants performed in the United
States?
How many stem cell transplants were
performed world wide in 2006?
What is the testament to the numerous
developments over the past few decades
in patient management before and after
transplant?
What else does the number of transplant
performed illustrate in advancements?
What critically important immunologic
mechanisms require continued
clarification?
Protein electrophoresis.
1. SPE shows monoclonal component -OR2. A significant quantitative abnormality of serum
immunoglobulins.
Immune deficiencies.
Polyclonal immunoglobulins.
Monoclonal immunoglobulins
One or more immunoglobulin classes.
Nephelometry
A bone aspirate and biopsy.
An autograft
Syngeneic graft
To another individual of the same species.
To another individual of a different species.
It can potentially be a life saving treatment for end
stage organ failure, cancers, autoimmune diseases,
immune deficiencies, and a variety of other diseases.
Over $28,000
$50,000
The number of transplants performed
The technologies for organ and stem cells acquisition
and sharing.
Mechanisms of graft rejection and graft-versusdisease.
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Immuno PPT Flashcards Unit 3
Specifically, what two components of
the immune system that promote
sustained graft survival are being
researched?
Transplantation immunology is the
largest immunologic barrier to
successful:
When does cell surface proteins play a
central role in immune recognition and
initiation of immune responses?
Why do allergenic responses result in
graft rejection in solid-organ and stem
cell transplantation or graft-versus-host
disease in stem cell transplantation?
When would an allogeneic response
within the recipient occur?
Classical (transplant) HLA antigens are
also know as:
What are the Class I HLA antigens?
What are the Class II HLA antigens?
Where is the encoding for HLA proteins
located?
HLA genes are inherited as
from
parental chromosomes.
Offspring receive
HLA haplotype
from each parent.
According to Mendelian inhertance,
there is a
chance of two siblings
inheriting the same two haplotypes, 50%
chance of being HLA
,
and a
chance of not sharing neither
HLA haplotype.
What does it meant to be:
1. HLA identical
2. HLA haploidentical
3. HLA non-identical
HLA proteins are
molecules.
Where are class I proteins expressed?
What is the product of the HLA-A,B,
and C genes?
What are co-dominantly expressed on
virtually all nucleated cells?
What is the products of the HLA-DRB1
1. The role of human leukocyte antigens (HLA)
2. The development of pharmacological agents that
interfere with various components of the immune
system
Allogeneic organ transplantation
Transplantation Immunology
The ubiquitous presence of cell surface proteins on
the surface of nucleated cells and their extensive
degree of polymorphism.
When there is a graft rejection in solid-organ and
stem cell transplantation or graft-versus-host disease
in stem cell transplantation.
Major histocompatibility antigens.
HLA-A, B, and C
HLA-DR, DQ, and DP
On the short arm of chromosome 6 in a set of closely
linked genes of the major histocompatibility complex
(MHC).
Haplotypes
One
1. 25%
2. haploidentical
3. 25%
1. Siblings share the same two haplotypes.
2. Siblings share one of two HLA haplotypes.
3. Siblings do not share HLA haplotypes.
Heterodimeric
On the cell surface covalently bound to beta-2microglobulin.
Class I Proteins
Class I heterodimers
Class II heterodimers.
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Immuno PPT Flashcards Unit 3
+ DRA1, HLA-DQB1 + DQA1, and
DPB1 + DPA1 genes?
Where are Class II heterodimers codominantly expressed?
Where do HLA proteins play a critical
role for the development and function of
the system?
How do HLA initiate adaptive immune
responses?
What serves as ligands for regulatory
receptors on natural killer cells in the
innate immune response?
The genes encoding the HLA proteins is
an extensive degree of:
What system is the most polymorphic
genetic system in humans?
Why polymorphism both considered an
advantage and disadvantage?
How were the second set of
transplantation antigens identified?
What disease was developed in the
studies that identified the second set of
transplantation antigens?
What results in a “slower” rejection
pace?
What is the name of second set of
transplantation antigens?
What are mHAs?
Where has encoding for mHAs been
identified?
How can you induce a recipient immune
response to the donor variant?
Primarily on antigen-presenting cells (example:
dendritic cells, monocytes, macrophages, B
lymphocytes.)
The innate and adaptive immune system.
They serve as recognition elements for antigen
receptors on T lymphocytes.
HLA proteins
Allelic polymorphism
HLA system
Enables populations to survive infectious challenges,
but severely restricts the ability to transplant foreign
tissue or cells between any two individuals.
Studies demonstrated tissue rejection in MHCidentical transplants and human stem cell transplants
between HLA-identical siblings.
Graft-versus-host disease
Minor Histocompatibility antigens (mHAs)
Minor Histocompatibility antigens (mHAs)
Non-HLA proteins that demonstrate polymorphism
in amino acid sequence within a species.
Both X-linked and autosomally.
By introducing a polymorphic variant of one of these
proteins from one individual into another individual
who possesses a different polymorphic variant.
Why does the recipient immune response CD4 and/or CD8 T cells recognize a variant protein
occur?
in the context of the recipient MHC molecule.
What is the recipient immune response
Foreign microbial antigen reaction
to the mHAs analogous to?
What mHAs have been identified?
1. Proteins encoded by the male Y chromosome
2. Proteins for which the recipient has homozygous
gene deletion.
3.Proteins that are autosomally encoded.
4. Proteins that are mitochondrial DNA encoded.
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Immuno PPT Flashcards Unit 3
Where are surface proteins that are
involved in gamma/delta T-cells
responses encoded?
Where can MIC proteins be expressed?
Where can’t MIC proteins be expressed?
When can MICA proteins serve as
targets?
Antibodies to MICA antigens have been
detected in as many as % of kidney
transplant patients.
What are MICA antibodies associated
with?
What is the only blood group system that
impacts clinical transplantation?
Anti-A or anti- B antibodies develop in
individuals lacking:
Why is ABO blood group
incompatibility a barrier to solid-organ
transplantation?
What can lead to hyperacute rejection of
the transplanted organ?
Why must recipient-donor pairs be ABO
identical or compatible?
An individual of blood group A will
posses anti-B antibodies, and can only
receive organ from an
donor.
A B-expressing individual has anti-A
antibodies and can only receive an
orgam from an
donor.
What has allowed the successful
transplantation of kidneys from ABOincompatible donors?
How is successful transplantation of
kidneys from ABO-incompatible donors
possible?
What other polymorphic genetic system
impacts allogeneic transplantation?
Who do the KIRs regulate?
How do KIRs regulate NK lymphocytes?
What governs the activity of the NK
cell?
What do NK cells do?
What class of MHC molecules are ligans
MHC class I-related chain A (MICA)
Endothelial cells, keratinocytes, fibroblasts, epithelial
cells, dendritic cells, and monocytes.
T or B lymphocytes
Allograft immune responses.
11%
Rejection episodes and decreased graft survival.
The ABO system.
The corresponding blood group antigens.
The antibodies can bind corresponding antigens
expressed on the vascular endothelium.
The complement cascade activated by ABO blood
group antibodies.
The antibodies can bind corresponding antigens
expressed on the vascular endothelium.
ABO-A or O
ABO-B or O
Plasma exchange and intravenous immunoglobulin
administration.
By lowering ABO antibody to levels that allow
transplantation to proceed without risk of hyperacute
rejection.
The killer Immunoglobulin-like receptor (KIR)
system.
Natural killer (NK) lymphocytes.
With the activating and inhibitory receptors that vary
in number and type on the any individual NK cell.
The balance of signals received by the activating and
inhibitory receptors.
NK cells secrete cytokines and non-MHC restricted
cytotoxicity.
MHC class I
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Immuno PPT Flashcards Unit 3
for the inhibitory KIRs?
As the NK cells encounter self class I
MHC proteins as it circulates the body,
what interaction allows for the NK cells
to maintain a quiet state?
How is the NK signal activated?
Where is the regulatory role of KIRs
being exploited?
How is the regulatory role of KIRs
helping in stem cell transplantation?
What is the result of receiving donor
inhibitory KIR?
What has shown to mediate a graftversus-leukemia reaction and prevent
relapse after transplantation?
Transplantation of cells or tissues
between two individuals is classified by:
Most transplantation falls into the
category of:
What will result in a vigorous immune
response to foreign MHC antigens and is
the primary stimulus to graft rejection?
How is the response to foreign MHC
antigens characterized?
What two distinct mechanisms enable
the recipient immune system to
recognize foreign HLA proteins?
What occurs in direct allorecognition?
How does direct allorecognition differ
from a typical T cell response to a
foreign antigen?
What factors can lead to a high
frequency T cell response?
How are T cells affected in a high
frequency response?
The
(MLR) is an invitro
correlate of direct allorecognition.
Other than direct allorecognition, how
does the immune system recognize
foreign HLA protein?
The interaction between MHC proteins and
inhibitory KIRs.
The NK cell encounters a reduction/lack of class I
expression, which allows for unoccupied inhibitory
receptors and an inhibitory signal loss occurs.
Haploidentical stem cell transplantation.
Recipients who lack corresponding class I MHC
protein receive the donor inhibitory KIR.
Alloreactivity by NK cells that repopulate the
recipient after transplantation.
Alloreactive NK cells
Genetic relatedness of the donor and the recipient.
Allografting.
HLA disparity between donor and recipient.
Strong cellular and humoral responses.
Direct and Indirect allorecognition.
Recipient T cells bind and respond directly to foreign
(allo) HLA proteins on graft cells.
The response is high frequency, up to 2% more T
cells respond.
Recognition of multiple amino acid disparities by
multiple T cell clones, the presence of multiple
different peptides on allogeneic that are each
recognized by different T cell clones, and the
presence of many foreign molecules per cells.
Activation with low affinity, which normally would
not be stimulated.
Mixed lymphocyte response.
The second pathway: indirect allorecognition.
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Immuno PPT Flashcards Unit 3
How is indirect allorecognition
analogous to the normal mechanism of
recognition of foreign antigens?
Indirect allorecognition plays a
predominant role in:
What does the effector response against
transplanted allogeneic tissue include?
How may an antibody result in cell
death?
What is variable in a rejection episode?
Name the three types of transplantation
rejection.
When does hyperacute rejection occur?
What mediates hyperacute rejection?
What may elicit a hyperacute rejection?
How does a hyperacute rejection lead to
a thrombus formation?
How does a thrombus formation affect
the transplanted tissue?
When is hyperacute rejection seldom
encountered?
Why are hyperacute rejection seldom
encountered in clinical transplantation?
How is the absence of donor HLA
specific antibodies confirmed prior to
transplantation?
What effect has crossmatch testing,
choosing ABO identical, and screening
for the presence of pre-formed HLA
antibodies on hyperacute rejection
episodes?
What complications can some
individuals who possess very low levels
of donor-specific antibody in the pretransplant period encounter?
What has the antibody-mediated
rejection that may take place over several
days termed?
It involves the uptake, processing, and presentation
of foreign HLA proteins by recipient antigenpresenting cells to recipient T cells.
Acute and chronic rejection.
Direct cytotoxicity, delayed-type hypersensitivity
responses, and antibody-mediated mechanisms.
It may mediate antibody-dependent cellular
cytotoxicity reactions and may fix complement.
The time of occurrence and the effector mechanism
that is operative.
1. hyperacute rejection
2. acute cellular rejection
3. chronic rejection
Within minutes to hours after the vascular supply to
the transplanted organ is established.
It is mediated by pre-formed antibody that react with
donor vascular endothelium.
ABO, HLA, and certain endothelial antigens.
With the binding of pre-formed antibodies to the
alloantigens that activate the complement cascade
and clotting mechanisms.
It can result in ischemia and necrosis of the
transplanted issue.
In a clinical transplantation.
Donor-recipient pairs are chosen to be ABO identical
or compatible, and patients awaiting transplantation
are screened for the presence of preformed HLA
antibodies.
The performance of a crossmatch test.
These approaches have virtually eliminated
hyperacute rejection episodes.
Antibody-mediated rejection may take place over
several days.
Accelerated rejection.
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Immuno PPT Flashcards Unit 3
What do hyperacute rejection and
accelerated rejection have in common?
How long does acute cellular rejection
take to develop?
Though acute cellular rejection is a
cellular-type rejection, what other
immunologic participant is also
involved?
What is characteristic of acute rejection?
What types of immunological cells are
predominately are found in interstitial
cellular infiltrates?
What roles do CD8+ and CD4 T cells
play in interstitial cellular infiltrates?
They both involve intravascular thrombosis and
necrosis of donor tissue.
Days to weeks after transplant.
Antibodies.
Parenchymal and vascular injury.
CD8+ T cells, CD4 T cells, and macrophages.
CD8+=Mediate cytotoxic reactions to foreign MHCexpressing cells
CD4= Produce cytokines and induce delayed-type
hypersensitivity (DTH) reactions.
What role do antibodies play in acute
Antibodies bind to vessel walls, activate
graft rejection?
complement, and induce transmural necrosis and
inflammation.
Do antibodies in hyperacute rejection
No.
and acute graft rejection play the same
Hyperacute rejection= create a thrombosis.
role?
Acute graft rejection= bind to vessel walls, activate
complement, and induce transmural necrosis and
inflammation
How has the development and
The response to alloantigens has improved early graft
application of potent immunosuppressive survival by reducing the incidence of acute rejection
drugs that target multiple pathways in
and providing approaches for its effective treatment.
the immune response affected solidorgan transplants?
What remains the most significant cause Chronic rejection.
of graft loss after the first year posttransplant?
Why is chronic rejection a significant
It is not readily amendable to treatment.
cause of graft loss?
What is characteristic of chronic
It is a process of graft arteriosclerosis characterized
rejection?
by progressive fibrosis, and scarring with narrowing
of the vessel lumen due to proliferation of smooth
muscle cells.
What are the predisposing factors that
 Prolonged cold ischemia.
impact the development of chronic
 Reperfusion.
rejection?
 Acute rejection episodes.
Toxicity from immunosuppressive drugs.
What is chronic rejection’s suspected
a) Delayed-type hypersensitivity reaction to
immunologic component?
foreign HLA proteins.
What allogeneic response uniquely
b) Graft-versus-host disease (GVHD).
complicates stem cell transplants, and
34
Immuno PPT Flashcards Unit 3
less commonly, lung and liver
transplants?
Why do recipients of stem cells
transplants for hematologic malignancies
typically have depleted bone marrow
prior to transplantation?
Where do the stem cells that are infused
for a transplant originate?
What is the benefit of the infused
products to contain some mature T cells?
How would mature T cells have a
negative effect to the transplant?
When does acute GVHD occur?
What is targeted in acute GVHD?
Compare what occurs if there is an
allogeneric mismatched stem cell
transplantation versus a matched stem
cell transplantation with GVHD.
How do infused T cells can mediate
GVHD?
What correlates the incidence and
severity of GVHD?
Why are all the below actions done?
 immunosuppressive therapy in
the early post-transplant.
removal of T lymphocytes from the
graph
How can T cell reduction have a
negative effect on the graft when it so
effective in lowering the incidence of
GVHD?
What can occur beyond 100 days posttransplant?
How does chronic GVHD resemble an
autoimmune disease?
What are some ways that
immunosuppressive agents are used?
How are immunosuppressive agents
usually used to prevent graft rejection?
Where is the growing list of agents used?
How are the immunosuppressive agents
used?
What are the negative effects of using
c) The chemotherapy used to treat the
malignancy.
d) Bone marrow or, more commonly, peripheral
blood stem cells.
e) Promotion of engraftment, reconstitution of
immunity, and mediation of a graft-versusleukemia effect.
f) Mature T cells may also mediate GVHD.
g) The first 100 days of post-infusion.
h) The skin, gastrointestinal tract, and liver.
Mismatched: mismatched HLA proteins targeted.
i) Matched: minor histocompatibility antigens
are targeted.
With massive release of cytokines due to large-scale
activation of the donor cells by MHC mismatched
proteins, and by infiltration and destruction of tissue.
The match status of the donor and recipient, and
other factors.
Reduce the incidence and severity of GVHD.
It can also reduce the graft-versus-leukemia (GBL)
effect of the infused cells, and increase the incidence
of graft failure.
Patients may experience chronic GVHD.
Fibrosis affects the skin, eyes, mouth, and other
mucosal surfaces.
Induction and maintenance of immune suppression
and treatment of rejection.
In combination of different immunosuppressive
agents.
To suppress anti-graft immune response in solidorgan and stem cell transplantation.
Induction and maintenance of immune suppression
and treatment of rejection.
Increased susceptibility to infection, malignancies,
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Immuno PPT Flashcards Unit 3
immunosuppressive agents?
What do the following have in common?
-corticosteroids
-Anti-metabolic agents
-calcineurin inhibitors
-polyclonal antibodies
What are corticosteroids?
What are corticosteroids use for in high
doses?
How do corticosteroids function in
immunosuppression?
What effect do corticosteroids have on
macrophages and leukocytes?
What complications may arise from
long-term use corticosteroids?
What interferes with the maturation of
lymphocytes and kills proliferating cells?
What was the first anti-metabolic agent
employed?
Why has mycophenolate mofetil
replaced the use of Azathioprine?
What do calineurin inhibitors do?
Name an example of a calcineurin
inhibitor.
How does inhibition of cytokine
synthesis affect T cells?
How does the block of T cell growth and
differentiation beneficial for graft
survival?
How does Rapamycin inhibit T cell
proliferation?
What binds to cell surface molecules on
the lymphocytes as induction agents and
to treat severe rejection episodes?
OKT3 is a mouse monoclonal antibody
that binds to the
on human
lymphocytes.
True or False.
The binding of OKT3 to the CD3 T-cells
surface has one outcome.
What may render the affected T cells
nonfunctional?
and other associated toxic side effects.
All are immunosuppressive antibodies.
Potent anti-inflammatory and immunosuppressive
agents used for immunosuppression maintenance.
To treat acute rejection episodes.
By blocking production and secretion of cytokines,
inflammatory mediators, chemo-attractants, and
adhesion molecules.
Decrease macrophage function and alter leukocytetrafficking patterns.
Hypertension and diabetes mellitus.
Anti-metabolic agents.
Azathioprine.
Mycophenolate mofetil has a more selective effect on
lymphocytes, and fewer side effects.
Block signal transduction in T lymphocytes, resulting
in impairment of cytokine synthesis, including IL-2,
3, 4, and interferon-Gamma.
Cyclosporine and FK-506 (tacrolimus)
Inhibition of cytokine synthesis blocks the growth
and differentiation of T cells.
It impairs the anti-graft response.
By binding to specific intracellular proteins,
including mammalian target of rapamycin (mTOR).
Monoclonal antibodies.
CD3 receptor
False.
Binding may modulate CD3 from the cell surface.
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Immuno PPT Flashcards Unit 3
How do higher doses of antibody deplete
T cells from circulation?
What problem is there with monoclonal
antibody preparations administered to
patient?
When are two polyclonal anti-T-cell
antibody preparations used?
Thymoglobulin is a an anti-thymocyte
antibody prepared in
.
ATGAM is a polyclonal antiserum
prepared from immunization of
.
Name the two immunosuppressive
agents that are potent enough to deplete
lymphocytes from the circulation.
What activity can the development of
these anti-mouse antibodies interfere
with?
What is the drawback associated with
administration of polyclonal antibody
preparations?
What are the two main activities carried
out by histocompatibility laboratories in
support of transplantation?
What is HLA typing?
For clinical HLA testing,
of
the classical transplant antigens or genes
are determined (HLA-A, B, Cw, DR,
DQ).
What information is used to find the
most suitable donor–recipient
combination from an immunologic
standpoint?
True or False.
Histocompatibility is the only
consideration given into the choice of a
particular donor for any given patient.
What is the classic procedure for
determining the HLA phenotype?
How are individuals HLA typed?
Purified
lymphocytes are used for
HLA class I typing.
Purified B lymphocytes are used for
With complement-mediated lysis or opsonization for
removal by phagocytic cells.
The development of anti-mouse antibodies by the
patient.
To treat severe rejection.
Rabbit.
Horses.
Thymoglobulin and ATGAM.
The activity of the monoclonal antibody.
The development of serum sickness due to antibody
responses to the foreign immunoglobulin.
HLA typing and HLA antibody
screening/identification.
The phenotypic or genotypic definition of the HLA
antigens or genes in a transplant candidate or donor.
Phenotypes or genotypes.
Histocomplatibility.
False.
The complement-dependent cytotoxicity (CDC) test.
Panels of antisera or monoclonal antibodies that
define individual or groups of immunologically
related HLA antigens are incubated with
lymphocytes from the individual.
T
Class II.
37
Immuno PPT Flashcards Unit 3
HLA
typing.
When is the complement added in the
complement-dependent cytotoxicity
(CDC) test?
Why is the dye added in the
complement-dependent cytotoxicity
(CDC) test?
What can provide an extensive array of
HLA antigens can be defined?
True or False.
There are several limitation to the CDC
method for HLA typing.
Why does the CDC method need viable
lymphocytes?
Separation of
is
required for definition of class I versus
class II antigens.
True or False.
The source of anti-sera for HLA typing
is not always consistent or reliable.
What effect does the source of anti-sera
have on reagents?
What is the ability to distinguished too
closely related yet distinct HLA antigens
called?
True or False.
The level of resolution is limited
Do the limits of resolution significantly
impact the role of HLA phenotyping for
matching solid-organ donors and
recipients?
When is a higher level of resolution
required?
Why are DNA-based (molecular) HLA
typing methods are now commonly
employed in histocompatibility
laboratories?
In clinical histocompatibility testing,
amplification is detected by:
Molecular-based HLA genotyping
methods use polymerase chain reaction
(PCR)–based amplification of HLA
genes followed by:
Which common approach to analysis
amplifies specific alleles or related allele
groups?
After incubation with antisera.
To distinguish live cells form dead when they are
viewed microscopically.
Complement-dependent cytotoxicity (CDC) test
True.
The CDC method demands timely performance of
the assay.
T and B lymphocytes
True.
The quality or quantity over time varies.
The level of resolution.
True.
No.
Unrelated stem cell transplantation.
They address the limitations of CDC-based methods.
Agarose gel electrophoresis.
Analysis of the amplified DNA to identify the
specific HLA allele or group of alleles.
PCR amplification of HLA genes with panels of
primer pairs.
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Immuno PPT Flashcards Unit 3
What detects the amplification of the
alleles or allele groups?
Which primer pairs result in the
detection of an amplification product?
How is the HLA type(s) determined?
What is referred to as generic
amplification?
What is the second common approach
for HLA approaching?
How is each specific or unique HLA
allele identified after amplification?
True or False.
Only those probes that specifically
hybridize to the amplified DNA will be
detected.
How is the HLA genotype determined?
What is the third common method for
HLA genotyping?
True or False.
HLA genotyping overcomes the
limitation of CDC-based HLA
phenotyping.
Do cells need to be viable to obtain DNA
for HLA genotyping?
What is the benefit of HLA genotyping
using chemically synthesized reagents?
HLA genotyping can provide varying
(
) that can be tailored to the
specific clinical need.
What results can DNA-based testing
provide?
What is required for matching of
unrelated stem cell donors and
recipients?
Antibodies to
can be detected in
candidates and recipients of solid-organ
transplants.
When can antibodies against HLA
antigens develop?
Why are patients awaiting solid-organ
transplantation are screened periodically
Agarose gel electrophoresis.
The primer pairs that bind to the target gene.
By indentifying which primers resulted in
amplification.
Performing a single PCR reaction that will amplify
all HLA gene variants at a specific locus.
Generic amplification.
The amplified gene is then subjected to hybridization
with a panel of DNA probes.
True.
Assessing which probes hybridized.
Sequencing of PCR-amplified HLA genes.
True.
No.
There is no reliance on human donors of anti-sera.
Levels of resolution
Results at a level of resolution comparable to CDCbased typing (antigen equivalent) or can provide
allele-level results.
Allele- level results from HLA genotyping.
HLA antigens
In response to multiple blood transfusions; two prior
HLA-mismatched transplants; and, in women, to
multiple pregnancies.
Because of the potential adverse impact HLA
antibodies can have on graft survival.
39
Immuno PPT Flashcards Unit 3
for HLA antibodies?
When is a donor eliminated for
consideration for donation to a specific
patient with specific HLA antibodies?
How often are patients tested for the
presence of HLA antibodies while they
are waiting for an organ offer?
Why is antibody screening and
identification also performed posttransplantation?
True or False.
The methods used for antibody detection
and identification have changed
significantly in recent years.
The CDC method used for
is
also used for HLA antibody detection
and identification.
When the CDC method is used for HLA
antibody detection and identification,
panels of lymphocytes with defined HLA
phenotypes are incubated with:
When will the cognate HLA antigen be
expressed?
How is the binding of the HLA antibody
to the panel of lymphocytes detected?
True or False.
In some scenarios, the level of antibody
in a patient serum may be below a level
detectable by the CDC assay.
When the donor has those HLA antigens that the
recipient possesses antibodies.
Monthly.
To aid in the diagnosis of antibody-mediated
rejection, and to assess the effectiveness of therapy
for antibody-mediated rejection.
True.
HLA typing
The patient’s serum.
When the patient serum contains HLA antibodies,
and binds with the panel of lymphocytes.
By addition of complement and a vital dye to assess
cell death microscopically.
True.
Why is anti-human globular (AHG)
added to a CDC assay?
To increase the test sensitivity because the AGHCDC assay can detect lower levels of antibody as
wells as isotypes of bound antibody that don’t
activate complement and thus wouldn't normally be
detected in the standard CDC assay.
What is referred as percent panel reactive The proportion of lymphocytes in the panel that are
antibody (%PRA)?
killed by the patient’s serum.
Usually how many unique lymphocyte
30-60
preparations are included in the panel?
How can the specificity of the antibodies Evaluating the phenotype of the panel cells.
be determined?
What has been developed as a substitute Enzyme-linked immunosorbent assay (ELISA)
for CDC-based HLA antibody testing?
What utilizes purified HLA antigens
ELISA assays
bound to the wells of microtiter plates?
40
Immuno PPT Flashcards Unit 3
When will patient serum added to the
wells of the plate bind to the antigen?
How is the bound antibody detected?
When is there a color change in an
ELISA assay?
What do the wells of the ELISA plate
provide because it may contain a pool of
HLA antigens?
How can ELISA be analogous to a CDCbased analysis by allowing percent PRA
and specificity to be determined?
Name another approach, not previously
discussed, for antibody detection and
identification.
Antibody in patient serum can be
incubated with latex beads that are
coated with:
True or False.
Flow cytometry can incubate either
single donor or a single purified HLA
protein.
How is the bound antibody in flow
cytometry detected?
What is the most sensitive method for
detecting HLA antibodies?
When flow cytometric methods can
provide the most specific determination
of the specificity of HLA antibodies?
What test is performed once a donor has
been identified for a particular patient?
Why donor–recipient crossmatch test is
performed?
Why donor lymphocytes are incubated
with recipient serum in a CDC assay?
What is the alternative way to detect
binding of antibody?
As for antibody screening and
identification, what is the most sensitive
method for detecting donor-specific
antibody?
How to define tumor immunology?
How is understood tumor immunology?
HLA-specific antibody is present.
With the addition of an enzyme-labeled antiimmunoglobulin reagent.
When the addition of the substrate detects bound
antibody in the wells.
Serve as a qualitative screen for the presence of HLA
antibody in a serum.
Each well of the ELISA may contain HLA antigens
representing a single donor.
Flow cytometry.
HLA antigens.
True.
By adding an FITC-labeled anti-IgG reagant.
Flow cytometric methods
When beads coated with a single HLA antigenic type
are used.
A donor–recipient crossmatch test.
To confirm the absence of donor-specific antibody.
To verify a lack of binding as detected by
microscopic analysis after addition of a vital dye.
By flow cytometry using an FITC-labeled anti- IgG
reagent.
The flow cytometric crossmatch
It is a study of the antigens associated with tumors,
the immune response to tumors, the tumor’s effect on
the host’s immune status, and the use of the immune
system to help eradicate the tumor
It is best understood with the background on
41
Immuno PPT Flashcards Unit 3
Why normal cell growth and division are
regulated processes?
How do we name the regulatory genes
that promote cell division?
What protooncogenes can cause?
What can cause tumors?
What cells form tumors?
If a tumor does not invade surrounding
tissue and normal body function is
largely preserved, it is said to be?
What tumors invade surrounding tissues
and greatly disrupt normal body
function?
What is the stage when the malignant
cells travel through the body, causing
new foci of malignancy until body
function is so disrupted that death
occurs?
How malignant cells typically differ
visually from normal cells?
differences between tumor cells and normal cells.
It is designed to rapidly produce new cells when
necessary, inhibit cell division when sufficient cells
are present, and limit cell lifespan (programmed cell
death, or apoptosis).
Protooncogenes
They uninhibit cell division if their expression is
altered or if they are mutated into oncogenes.
Mutations or malfunctions in tumor suppressor genes
that remove growth-inhibitory signals.
Cells that possess many of the attributes of the
normal
cells from which they arose but have accelerated or
dysregulated growth.
Benign tumor.
Malignant tumors.
Metastasis.
They are metabolically more active to support their
growth, and express different genes or different
levels of gene products as compared to normal cells.
Leukemic cells.
What cells have aberrant morphology
and express different surface antigens
either in type or amount?
Is the conversion of a normal cell to a
It is a process.
malignant cell is typically a process, or
an event?
What is the phase when cells are exposed Induction phase.
to a variety of environmental insults,
including chemical carcinogens,
oncogenic viruses, and radiation
(ionizing and ultraviolet)?
Why cancer is developed?
It is the result of multiple mutations caused by these
insults.
In what cells cancer can develop faster?
It more readily develops in cells genetically
predisposed to mutations.
How long takes the induction phase?
It may take months to years.
What happens during the induction
Cells exhibit dysplasia or abnormal growth that is not
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Immuno PPT Flashcards Unit 3
phase?
What is the phase of cancer when
neoplastic cells have formed but are
confined to the tissue of origin?
When cells are malignant, the cancer
proceeds to what phase?
What happens during the invasion
phase?
Why detection is difficult in the early
stages?
yet considered neoplasia, or consistent with a tumor.
In situ phase.
Invasion phase.
Cancer proceeds to dissemination throughout the
body, usually via the blood and lymphatics.
There are fewer cells to detect and they more closely
resemble normal cells if they are dysplastic rather
than neoplastic.
The progeny of the cell that undergoes
transformation are monoclonal in origin.
Rapid uncontrolled proliferation.
Why cells are initially identical
phenotypically and genotypically?
What is the cause of DNA replication,
developing cellular phenotypic and
genotypic heterogeneity?
What helps cancer cells escape from both The ability to mutate.
the immune system and from
chemotherapeutic agen?
What is the complication of mutation?
It complicates identification of reliable tumor
markers, as marker expression may change over
time.
What is the classification of tumors that
Poorly differentiated, or anaplastic tumors.
are more similar to fetal or embryonic
tissue?
What is the classification of tumors that
Well-differentiated tumors.
are more similar to normal tissue?
What tumors are more aggressive and
Poorly differentiated tumors.
lead to poorer patient prognosis?
What is the meaning of the TNM system. Classification of tumors by the size of the primary
tumor (T), the involvement of adjacent lymph nodes
(N), and the detection of metastasis (M).
What is the term used to describe the
Immunosurveillance.
processes by which cells of the immune
system look for and recognise foreign
pathoges such as bacteria and viruses, or
pre-cancerous and cancerous cells in the
body?
Where do we see increased incidence of In individuals with deficient immune systems such as
tumors formation?
the elderly and in immunosuppressed individuals, but
this is not proof of the existence of
Immunosurveillance.
What is the cause of tumors
Increased lifespan implies increased exposure to
development?
carcinogens.
In what individuals many tumors are
In immunosuppressed people.
essentially infections, as they are of viral
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Immuno PPT Flashcards Unit 3
rather than spontaneous origin?
Why tumors in immunosuppressed
people are infectious?
Why would the incidence of nonviral
tumors in T cell-deficient individuals be
not increased?
What cell are present in some tumors,
and are associated with a better
prognosis?
What is the common characteristic of
many tumors that allows tumor cells to
escape from T cells?
What is the work of some successful
therapeutic advances?
What do we observe in certain
therapeutic advances?
Why it is possible that
Immunosurveillance itself is ultimately
responsible for tumors that can escape
the immune system?
When it is important to determine
mechanisms by which tumors escape?
When some tumor antigens may be
poorly immunogenic?
What tumor cell may lack?
What kind of resistance can be observed
in tumors in people with deficient
immune systems?
What prevents interaction with the tumor
cell?
What other elements cause some tumors
to be immunosuppressive?
What are the local environments?
In what phase of immunosurveillance,
tumors are sufficiently immunogenic to
be eliminated by the immune system?
During what stage as mutations occur
over time, cells that are less
immunogenic have a growth advantage?
In what phase cancer cells have mutated
beyond the immune system's ability to
control them?
What research has been made of tumor
immunosurveillance?
Because they are of viral rather than spontaneous
origin.
This may be due to adequate NK cell activity,
although these topics are still under study.
NK cells, T lymphocytes (tumor infiltrating
lymphocytes [TIL]), and macrophage infiltrates.
Loss of MHC expression and subsequent poor
antigen presentation.
They are directed toward upregulating the immune
system to fight a particular cancer.
Spontaneous regression of some tumors.
It is because of immunoediting.
If Immunosurveillance is indeed occurring.
If they are very similar to normal self antigens and
induce immune tolerance.
MHC class I, class II, or accessory molecule
expression.
Resistant to the immune response, or the tumor's
growth rate regulation by the immune system.
When soluble antigen released by the tumor may
bind to the T cell receptor.
Local environment.
Immunosuppressive cytokines such as transforming
growth factor-beta.
Elimination phase.
Equilibrium stage.
Escape phase.
To immediately determine the extent and precise
mechanisms.
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Immuno PPT Flashcards Unit 3
What research is still ongoing?
What antigens are present in the tumor
tissue in higher amounts than in normal
tissue?
What are the products of mutated genes
and viruses?
What is the other way that tumorassociated antigens can be present?
What antigens are most highly expressed
in both normally developing fetal tissue
and in certain kinds of cancers?
Why virtually no tumor-associated
antigens are tumor specific?
What is the perfect tumor-associated
antigen needed for detection?
What tests are used in ostensibly normal
people to detect occult cancer?
What tests are those that help determine
differential diagnosis, tumor stage,
prognosis, and therapy selection?
What profoundly impacts the test’s
usefulness?
What supports the probability
calculation?
What are the points in Bayes’ theorem?
What it means 99% sensitivity and 95%
specificity?
What if the cancer rate in the population
is 0.1%?
What if the cancer rate in the population
is 1%?
What if a clinician can identify this
cancer by signs and symptoms 75% of
the time?
Why tests for differential diagnosis,
generally perform relatively well?
What are the presumptions for
screening tests?
Research into the manipulation of the immune
system to fight cancers.
Tumor-associated antigens (TAA).
Tumor-associated antigens (TAA).
They can also arise from aberrant expression of
normal genes.
Oncofetal tumor antigens.
Because they also have been found in some
noncancerous human tissue.
It should be unique to a particular timber could aid in
the screening, diagnosis, history of pathic evaluation,
staging, monitoring, localization, and
immunotherapy of various malignancies
Screening tests.
Diagnostic tests.
Disease prevalence.
Bayes’ theorem.
A “good” cancer test with 99% sensitivity and 95%
specificity.
Test will be positive in 99 out of 100 people with
disease, and it will be negative in 95 out of 100
people without disease.
Then 98 percent of positives would be false
positives.
The false-positive rate is still 83 percent.
The false-positive rate is 1.7 percent.
Because the clinical suspicion of cancer translates to
a higher cancer prevalence in the population being
tested.
Relatively low number of people being screened
actually have cancer and that it would be worse to
miss a cancer then to do further testing on a normal
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Immuno PPT Flashcards Unit 3
Why the concept of a normal or
reference range does not really apply?
What type of values are typically
selected above the point at which further
testing will be done?
How are the cutoff values for screening
tests generally set?
person to exclude cancer.
It may be difficult to determine with certainty that a
reference population does not have cancer, and
values from normal and cancerous populations may
overlap.
Cutoff values for tumor markers.
These are set with the expectation that there will be
an extremely high number of false positives due to
low disease prevalence.
How can the additional testing be?
Invasive, costly, or anxiety-provoking.
What conditions are needed for
The tumor is an important health problem, there is a
widespread use of a laboratory test to
recognizable early symptom or marker that can be
screen for cancer?
used for screening with reasonably high sensitivity
and specificity
What is included in the cost of laboratory Longer morbidity in patients whose prognosis is not
tests?
changed, overtreatment of questionable diagnoses,
misleading reassurance for those with false-negative
results, and anxiety and possible morbidity from
more invasive testing for those with false positive
results.
What is the principle of lab test?
It is a tumor for which treatment at an early stage is
more successful than at a later stage.
What are the advantages of tests?
Costs and benefits of the screening test are
acceptable to the population; including improved
survival time, less radical treatment needed for
tumors detected earlier, and reassurance for those
with negative results.
What includes cost of lab tests?
Longer morbidity in patients whose prognosis is not
changed, over treatment of questionable diagnoses,
misleading reassurance for those with false-negative
results, anxiety and possible morbidity from more
invasive testing for those with false-positive results,
the actual physical hazards of the screening test, and
the actual dollar costs of the screening test.
What needs to be done to improve the
Selected subgroups, such as patients with a family
cost-to-benefit ratio?
history of cancer, should be screened when possible
instead of the entire population.
How differential diagnosis of tumor type By tissue/cell morphology and detection of tumor
can be done?
markers directly from tumor tissue.
What techniques are required for
Immunohistochemistry; detection of expressed
detection of tumor antigens?
antigens using labeled antibodies; and fluorescent in
situ hybridization (FISH).
What can be detected by
Expressed antigens using labeled antibodies, and
immunohistochemistry?
molecular techniques such as fluorescent in situ
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Immuno PPT Flashcards Unit 3
What can be detected by FISH?
What is the principle of lab test?
What can be helpful in pathological
diagnosis?
Why markers must be combined with
other clinical results?
What is relatively common in
performing lab test using markers?
What can happen if the DNA changes in
malignant transformation?
How is done the disease management
with laboratory tests?
What is established for the lab test?
What is done if the disease and
treatments progress?
What is important in clinical usage of
tumor markers?
What must be done by the same
methodology so that changes are due to
actual alterations in the patient, not
differences in methods?
What are the dilemmas associated with
tumor markers.
Why detection of PSA is very specific
for the prostate gland and increases in
almost all prostate cancers?
How is the production of PSA related in
a healthy men?
What may happen when men age?
hybridization (FISH).
Normal gene expression using nucleic acid probes.
Differential diagnosis by the pathologist are less
stringent than the requirements for using tests for
widespread screening.
The marker must be differentially expressed in the
tumor of origin and other tumors, which may have
similar appearance histologically.
The differentiation that occurs with transformation
sometimes can result in loss of the marker.
False-negative results.
This sometimes can cause expression of a marker
that is not normally associated with the tumor type in
question, although this occurrence is relatively
uncommon.
It is typically done with serial determinations of a
tumor marker.
A baseline level at initial diagnosis.
Additional levels are determined to establish
prognosis, monitor the results of therapy, and detect
recurrence.
It is not the absolute value of the tumor marker that is
important but rather the upward or downward trend
when the marker’s biological half-life is considered.
Serial determinations done to aid the clinician in
making important decisions concerning the
therapeutic regimen.
Problems with prostate-specific antigen (PSA).
It is because no other tissue in men is known to
produce PSA.
The amount of PSA produced is directly related to
the glands size.
Many men developed benign enlarged prostate,
further, they are more likely to develop prostate
cancer, but they are less likely to die from it.
What sometimes should be done if as
There are prostate cancers that can and should be left
men age and develop prostate cancers?
alone.
What is recommended for PSA screening It should be done once a man's remaining life
cease?
expectancy is less than 10 years.
What has been done in lab testing for
It is possible to discriminate between benign
PSA?
prostatic hypertrophy, weekly aggressive cancers,
and highly aggressive cancers using PSA.
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Immuno PPT Flashcards Unit 3
What is more associated with cancer and
his justification for a biopsy?
Why the net benefit to the widespread
PSA screening currently done in the
United States a be questionable?
What are the variety of methods that
clinicians screen for the presence of
malignancies?
What is the advantage of laboratory
tests?
What are the three types of laboratory
methods for cancer screening and
diagnosis?
Why the choice of method often depends
on convenience, cost, sensitivity, and
specificity?
How pathologist and histology labs
process suspected tumor tissue?
What is the process to enhance the
visible features?
What is the feature of evaluation of
morphology and staining patterns?
What is required to accurately diagnose
cancer by morphology alone?
How is the final diagnosis often made?
What include some of the molecular
diagnostic techniques that have become
increasingly routine?
What is the purpose of cytogenetics
studies?
What is the purpose of nucleic acid
amplification techniques?
What is the purpose of fluorescent in situ
If the free-to-bound ratio of PSA is low or the rate of
PSA is increasing at a rate that exceeds 0.5 NG/ML
per year (PSA velocity).
It is due to the fact that an increased PSA does not
always indicate a cancerous state or an aggressive
cancer that must be treated.
Commonly used tests include stool occult blood and
colonoscopy for colorectal carcinoma, tests for
cervical cancer, self-exams for breast and testicular
cancer, mammogram for breast cancer, and digital
rectal exam for prostate cancer.
These tests can provide important adjunct
information to patient histories and physical
examinations.
These are gross and microscopic morphology of
tumors; detection of antigen/protein tumor markers;
and DNA/RNA molecular diagnostics.
Because these techniques are complementary in that
many of the DNA changes and subsequent mRNA
expression result in the altered antigens/proteins
detected or morphology visualized.
It is done with gross dissection and preparation of
slides for microscopic analysis.
A variety of special stains, nucleic acid probes, and
tumor marker antibodies can be applied to the slides.
It can be very subjective, and classification
categories can be rather broad.
Considerable skill.
It is done with supplemental clinical information and
additional testing.
These are cytogenetic studies; nucleic acid
amplification techniques by polymerase chain
reaction (PCR) and its variants; and fluorescent in
situ hybridization (FISH).
More precise knowledge of the exact gene defects
present in various cancers is gained, testing for the
aberrant genes is becoming prevalent.
Polymerize chain reaction (PCR) and its variants
increase the inherent level of DNA or RNA, allowing
the detection of small populations of cancer cells
(including circulating cells in metastatic sis) and the
detection of mutagens, deletions, and gene
rearrangements/translocations.
Nucleic acid probes capable of binding to sequences
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Immuno PPT Flashcards Unit 3
hybridization (FISH)?
What are other similar techniques using
non-fluorescent labels?
What tests for genetic screening of
cancers are available?
What available marker for CML is a
well-respected?
What is almost exclusively present in
multiple myeloma or other lymphoid
malignancy?
What is the cause of most other
phenotypically related cancers?
What are the future tests that are
currently being developed with multiple
nucleic acid tests contained on a single
chip to allow for simultaneous testing of
a sample for multiple genes?
What is the potential use of micro-array
tests?
What are the genetic abnormalities
associated with an increased risk of
developing a cancer or with a poorer
prognosis?
What is an example of a prognostic
marker?
What is the feature of Her2/neu
oncogene in breast cancers?
What are the characteristics of ideal
tumor marker?
What are other characteristics of ideal
tumor marker?
What are other characteristics of ideal
tumor marker?
What are the characteristics of ideal
tumor marker?
What are the seven categories of tumor
markers detection?
of interest are tagged with fluorophores and applied
to cells. Cells containing the sequence of interest can
be visualized with fluorescent microscopes.
Enzymes and silver stains.
DNA/RNA sequences.
The BCR-ABL translocation.
Monoclonal expression of B cell DNA
rearrangement.
They have heterogeneous genetic causes, so
universal and reliable genetic abnormalities are not
yet described.
Micro-array test.
Detection and semi quantitation of mRNA expression
in cells to distinguish patterns (rather than single
markers) consistent with cancer.
Susceptibility genes like the BRCA-1 and BRCA-2
mutations linked with an increased risk of breast,
ovarian, and prostate cancers.
Overexpression of the Her2/neu oncogene.
It tend to be more aggressive but will more likely
respond to certain therapies (trastuzumab).
It must be produced by the tumor or as a result of the
tumor and must be secreted into some biological
fluid for analysis.
Its circulating half-life must be long enough to permit
its concentration to rise with increasing tumor load.
It must increase to clinically significant levels (above
background control levels) while the disease is still
treatable and with few false negatives (sufficient
sensitivity).
The antigen must be absent from or at background
levels in all individuals without the malignant disease
in question to minimize false-positive test results
(sufficient specificity).
Cell surface markers, proteins, oncofetal antigens,
carbohydrate antigens, blood group androgens,
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Immuno PPT Flashcards Unit 3
How are most of these makers detected?
Why tumor markers are not always
directly associated with the malignant
transformation?
What is an example of these tumors?
How many tumor markers are approved
by FDA?
What tests are used with a notation on
the lab report stating that the results are
for research use only
Who has developed a set of very useful
consensus guidelines regarding the
clinical use of tumor markers?
What the National Academy of Clinical
Biochemistry has on their list?
What current testing guidelines
recommend?
What is used to identify and quantify an
array of proteins simultaneously present
in a sample?
What is the new field in tumor markers
this is currently only at the research
stage?
What is the purpose of protein profiling
in cancer patients?
enzymes/iso enzymes, and hormones.
By immunologic methods with antibodies to distinct
epitopes on the molecules.
Often, they are the normal products of tissue of
origin being expressed, and this is more likely if the
tumor is well differentiated.
Endocrine gland tumors often produce generous
amounts of hormone that the tissue of origin
produces.
Less than a dozen.
Non-FDA-approved markers.
The National Academy of Clinical Biochemistry.
Methods and markers for a variety of purposes that
have acceptable evidence of validity.
Very few markers for screening/early detection and
still recommend using adjunct tests or screening
high-risk populations.
Mass spectrometry (MS).
Oncopeptidomics.
It will aid in the discovery of new tumor markers or
patterns of protein expression that are consistent with
cancer.
What is the purpose of oncopeptidomics? It may allow more subtle increases of tumor markers
to have diagnostic significance, since multiple
markers can be measured and the overall pattern
assessed, but this is currently only at the research
stage.
What are some important aspects to
Most tumor markers are detected using antibodies
laboratory testing for tumor markers?
because of the specificity of antibodies and the
general reliability of immunoassays.
Why there are some important
Antibodies are directed at specific epitopes, and the
limitations to using antibodies as
antibodies from different manufacturers may vary
reagents?
greatly in terms of what is measured, particularly if
monoclonal antibodies are used.
Why it important to use the same method Because antibodies from different manufacturers
for monitoring patients over time, and
may vary greatly in terms of what is measured.
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Immuno PPT Flashcards Unit 3
clinicians should be aware of this if
patients change clinics or laboratories?
What must be done if laboratories switch
methods?
What is the specificity of antibodies
employed in tumor marker assays?
What is particularly problematic when
antibodies are employed in tumor marker
assays?
What some tumors may produce?
What is the phenomenon similar to the
prozone in immunoassays?
Why it is critical that criteria be
developed to identify situations in which
the hook effect may be present?
What are other related problem of
antigen excess in automated systems?
Why heterophile antibodies in
specimens can interfere profoundly with
results?
What happened in a tragic case involving
false-positive hCG results from an
automated analyzer?
With what antibodies false increases and
false decreases are associated?
What is the purpose of commercially
available antibody-blocking reagents?
Why specimen that may have heterophile
antibodies should not be reported until
the issue is resolved?
Whatis the final aspect of tumor
immunology to be discussed?
What aspect has long intrigued scientist?
What are the two types of
immunotherapeutic methods?
What is the method that involves transfer
of antibody, cytokines, or cells to
patients who may not be able to mount
an immune response?
What is the method that patients are
treated in a manner that stimulates them
They must provide a transition period during which
specimens are measured by both methods and
specimens are archived until new data is established
for each patient.
It is not absolute.
Antibodies will cross-react with similar structures
and there is problem when these are in excessive
amounts, as can occur in cancer.
Massive amounts of tumor marker molecules.
It has been called the high-dose hook effect.
Specimens can be diluted and accurate results
obtained.
It is specimen carryover, so in addition to diluting the
specimen with excessive antigen, the specimen being
tested immediately after it may need to be repeated.
Because many of the antibodies used in
immunoassays are animal in origin.
Several women had unnecessary chemotherapy or
hysterectomies for presumed undetected cancer.
Heterophile antibodies.
They block heterophile antibodies in suspicious
specimens.
Specimens exhibiting nonlinear behavior on dilution
or with discrepant results using different methods or
after applying antibody-blocking reagents.
Immunotherapy.
The possibility of stimulating the patient’s own
immune system to respond to tumor-associated
antigens.
Passive or active immunotherapy.
Passive immunotherapy.
Active immunotherapy.
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Immuno PPT Flashcards Unit 3
to mount immune responses to their
tumors?
Why passive transfer of allogeneric
cellular immunity from one person to
another to fight cancer has many
barriers?
What is more likely to be successful than
passive transfer?
What method brings improved patient
prognosis?
What method is theoretically possible?
What is the model of adoptive T-cell
therapy?
What is the reason for recipients to be
immunosuppressed?
What is the one strategy in this model to
treat GVHD?
What happens when allergenic T-cells
are genetically engineered?
What are the other strategies for adoptive
T-cell therapy?
Why patient is lymphodepleted?
What other cells can be harvested?
Why new lines attempts have also been
made?
What is mostly used for passive transfer
of antibody to treat cancer?
What could be induced against "Naked"
monoclonal antibodies against cancer?
What could trigger antibodies if they are
directed towards particular receptors?
What are the antibodies conjugated to
toxins or radioisotopes on the premise
that they can kill cancer cells while
leaving adjacent cells intact.
What is needed for the passive
immunotherapy to work?
What is needed for the passive
immunotherapy to work?
What is needed for the passive
Because of possible recipient rejection of foreign
cells, graft-versus-host disease, and the fragility of
live cells, although research models are being
studied.
Inducing a patient's own cellular immunity.
GVHD called graft versus leukemia that has been
demonstrated with transfer of allogeneric T cells.
Successful passive transfer of anticancer T cells.
T cells from allogeneric donors can be immunized
against tumors.
They receive T-cells to prevent rejection and to
eliminate T suppressor mechanisms.
It is to genetically engineer the allergenic T cells
with a "suicide switch".
This genes make cells vulnerable to a drug that will
immediately eliminate them in the event of GVHD.
Use of autologous T cells, tumor-infiltrating
lymphocytes (TILs) can be harvested and expanded
in vitro using IL-2.
To remove T suppressor cells, and high concentration
of TILs are transfused.
Autologous T cells that are exposed to cancer
antigens, expanded with IL-2, and then returned to
the patient.
To insert genetically engineered T-cell receptors into
autologous T cells.
Monoclonal antibodies.
Antibody -dependent cell-mediated cytolysis
(ADCC), complement-mediated lysis, or
opsonization.
Desirable action in the cell such as inducing
apoptosis or inhibiting growth signals.
Antibody conjugates, or immunotoxins.
Antibodies must be directed at a cell surface antigen
with high density.
The antigen must be present on the primary tumor
and on all the metastatic foci.
Normal tissues must be free from the antigen or not
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Immuno PPT Flashcards Unit 3
immunotherapy to work?
What is needed for the passive
immunotherapy to work?
What are some obstacles involved in
immunotherapy with antibodies?
What other obstacles could be involved
in immunotherapy with antibodies?
What is significant in patients receiving
therapy?
Immunotherapeutic antibodies are most
effective against what diseases?
Why antibodies poorly penetrate tumor
mass?
Why antibodies are rarely, if ever, used
alone?
What is usually recommended in treating
tumors?
Why radiolabeled antibodies are
particularly effective?
Why radiolabeled antibodies are
advantageous for tumors with
heterogeneous antigen expression?
What is the additional use for
radiolabeled antibodies?
Why the usage of radiolabeled antibodies
must be managed?
Are there any FDA-approved antibodytoxin conjugates available?
How conjugation can theoretically allow
the use of ”ultratoxic" drugs and some
extreme cytotoxins?
What cytotoxins are under study?
Why antibodies must bypass the normal
susceptible to the toxin.
The antibodies must have sufficient access to the
tumor tissue.
Tumor heterogeneity with regard to antigenic
expression; antigenic modulation or the loss of
antigen from the tumor cells; failure of antibodies to
penetrate tumor tissue and failure of antibody-toxin
conjugates to internalize into the cell after binding
and release of toxins.
Toxic effects on other tissues, particularly the
hematopoietic organs; the limited amount of toxin
that can be linked to the antibody without destruction
of binding activity; host immune response to the
injected antibody and circulating antigen forming
immune complexes with the antibodies, removing
them from circulation.
Development of heterophile antibodies.
Hematologic malignancies, small tumors, and micro
metastases, not bulky tumors.
Because they are large molecules, and they bind to
the first available antigen encountered on the outside
of the tumor.
Since there is usually more than one path for cell
growth and surgical removal or debulking of a tumor
is also possible.
Combination therapy with chemotherapeutic agents
or other treatments.
Because of the "bystander" or "crossfire" effect seen
with high-energy isotopes that can kill up to several
hundred cells.
It could allow antibodies to kill cells that are not
expressing antigen at all.
Imaging studies to locate foci of cancer.
To minimize bone marrow toxicity, although this
toxicity is generally reversible.
No, besides one substance for T cell lymphoma.
Because the agents delivery is limited and focused by
the antibody.
Diphtheria toxin, Pseudomonas exotoxin, abrin, ricin
and saporin.
Because toxins have their own binding mechanisms.
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Immuno PPT Flashcards Unit 3
mechanism or the toxin must be
modified?
Why some cytotoxins must be
internalized to be effective?
What is the goal of active
immunotherapy?
What is used as nonspecific stimulation
in active immunotherapy?
What is still treated by Bacillus Calmette
Guerin (BCG)?
What is the use of novel adjuvants and
selective use of stimulatory cytokines
(TNF-α, IFN-γ, IL-1, IL-2)?
What are other attempts at stimulating
host immune systems?
What is used for stimulation of immune
system?
Why cancer vaccinations have been of
great interest to researchers?
So the antibody must target an epitope that would be
internalized.
It is to have the patient develop an immune response
that will help eliminate the tumor.
Adjuvants such as Bacillus Calmette Guerin (BCG).
Superficial bladder cancer.
In immunocompetent patients to enhance the natural
antitumor response and the artificial vaccine-induced
response.
Transfection of normal cells or isolated tumor cells
with genes for cytokine production and injection of
the modified cells into or around the tumor.
This has been done with many cytokines.
When specific viruses are associated with the cancer,
vaccine construction is relatively straightforward,
since viral antigens are obviously foreign.
What is an excellent example of cancer
The vaccine for human papilloma virus "HPV" to
vaccines?
prevent cervical cancer.
Why vaccines must be protective against Many viruses have several serotypes and not all of
the appropriate epitopes?
which may be associated with cancer.
What is the feature of HPV vaccines?
They are directed epitopes that prevent initial
infection with carcinogenic serotypes but do not help
treat established cervical cancer, as these epitopes are
down regulated in cancer cells.
Is there a distinction between
Yes.
prophylactic vaccines and therapeutic
ones?
Why prophylactic vaccination is more
Since many of the antigens expressed on tumors,
difficult in the absence of a viral cause of appear to some degree on normal tissue.
cancers?
What cells are often deleted by tolerance Hi-affinity cytotoxic T lymphocytes against tumorpathways?
associated antigens (TAA).
Why the expression of an antigen on a
Since coexpression with MHC I and obligatory
tumor does not automatically make it a
accessory molecules is required for adequate T cell
suitable vaccine target?
response.
Why vaccination with tumor lysates and Due to the heterogeneity of antigens presented on
peptide antigen vaccines have had
tumors
limited success?
Why vaccination with tumor lysates and Due to the few "public antigens" common to all
peptide antigen vaccines have had
tumors
limited success?
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Immuno PPT Flashcards Unit 3
Why vaccination with tumor lysates and
peptide antigen vaccines have had
limited success?
What is more difficult in designing
vaccines?
What various strategies have been
attempted to identify sufficiently
immunogenic antigens and how to
present them to T cells?
What is prime dendritic cells?
What immunity can stimulate the
strategy to prime dendritic cells?
What can stimulate the strategy to prime
dendritic cells?
What is the general principle of prime
dendritic cells technique?
How should be done antigen exposure in
prime dendritic cells technique?
How should be done antigen exposure in
prime dendritic cells technique?
How should be done antigen exposure in
prime dendritic cells technique?
How should be done antigen exposure in
prime dendritic cells technique?
How should be done antigen exposure in
prime dendritic cells technique?
How the DC's are reintroduced in a
patient?
What are needed to demonstrate
completely success vaccines?
What are needed to demonstrate
completely success vaccines?
What are needed to demonstrate
completely success vaccines?
Why are immunization protocols
important?
What is the first step of traditional tumor
therapy?
In tumor therapy what will eradicate
immune system after tumors will be debulked?
What is the reason of active study and
increased optimism in recent years?
The specific immune response to
bacterial infections includes formation of
what?
Due to the many "private antigens" you need to an
individual's tumor.
Designing custom vaccines for each individual
The strategy to prime dendritic cells
Particularly potent antigen-presenting cells
Both: humoral and cellular
Immune tolerance reactions
DC line is cultured from the patient and then exposed
to tumor antigen
By using co-culture with purified tumor antigens
By using co-culture with purified tumor lysate
By using fusion of DC's with tumor cells
By using DC phagocytosis of dead tumor cells
By using transfection of RNA
Intravenously, subcutaneously, etc. as a vaccine
The details of optimal antigens
DC priming
Modes of DC delivery
Protocols are important adjunct to traditional
therapies
Tumors will first be de-bulked
Residual tumor and micro metastases
The increased understanding of tumor immunology
antibodies
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Immuno PPT Flashcards Unit 3
Antibodies in a response to bacterial
infection are produced to what?
Antibody formation is the main defense
against what bacteria?
What is helpful in attacking intracellular
bacteria?
Why Bacteria have developed several
ways?
Why Bacteria have developed several
ways?
What is one of the mechanism of
bacterial development to inhibit immune
response?
What is one of the mechanism of
bacterial development to inhibit immune
response?
What is one of the mechanism of
bacterial development to inhibit immune
response?
How does the mechanism of avoiding
the effects of antibody occur?
The mechanism of avoiding the effects
of antibody through altering bacterial
antigens (epitopes) as a result of what?
How some bacteria can avoid effect of
antibodies?
How some bacteria can avoid effect of
antibodies?
What is a target of most of the evasion
mechanisms of bacteria?
What are the stages of bacterial defense
in the process of phagocytosis?
What is an additional mechanism of
resisting digestion?
What are trigger the release of lysosomal
contents into the cytoplasm of the
phagocytic cells?
What is a result of the release of
lysosomal contents into the cytoplasm of
the phagocytic cells?
What is the major defense of some
bacteria?
Gram-positive spherical, ovoid, or
lancet-shaped organisms are
Bacteria that catalase negative and are
often seen in pairs or chains are
to exotoxins or other secreted bacterial products
extracellular bacteria
cell-mediated immunity
to inhibit the immune response
make it more difficult for the immune response to
occur
avoiding antibody
blocking phagocytosis
inactivating the complement cascade
through altering bacterial antigens (epitopes)
genetic mutations
By down-regulation of MHC molecules
produce proteases that degrade IgA
the process of phagocytosis
chemotaxis, adhesion, and digestion
production of toxins
production of toxins
Killing these cells
to block the action of complement
Streptococci
Streptococci
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Immuno PPT Flashcards Unit 3
Streptococci are divided into groups or
serotypes on the basis of what?
What cell wall components are the basis
for dividing Streptococci into groups?
Interior to the protein layer is
How many defined groups are divided
Streptococci by the group-specific
carbohydrate?
How are 20 groups of Streptococci
designated?
What is the name of Streptococci groups
that are divided by group-specific
carbohydrate?
What do some strains possess outside the
cell wall?
What does contribute to the bacterium’s
antiphagocytic properties?
What are additional virulence factors?
What are exoantigens or exotoxins?
Proteins excreted by the bacterial cells as
they metabolize during the course of
streptococcal infections are
Detection of host antibodies to exotoxins
is important in the diagnosis of what
disease?
Antibodies are produced to what
exoantigens or exotoxins?
Antibodies are produced to what
exoantigens or exotoxins?
Antibodies are produced to what
exoantigens or exotoxins?
Antibodies are produced to what
exoantigens or exotoxins?
Antibodies are produced to what
exoantigens or exotoxins?
What diagnosis must be used to identify
rheumatic fever and glomerulonephritis?
Why do serological diagnosis used to
identify rheumatic fever and
glomerulonephritis?
What do group A streptococci elaborate?
The antibody response to one or more of
exotoxins of group A streptococci is
used as
The antibody response to streptococcal
products is variable due to what factor?
certain cell wall components
M and T proteins
the group-specific carbohydrate
20
A–H and K–V
Lancefield groups
hyaluronic acid capsule
a hyaluronic acid capsule outside the cell wall
Exoantigens or exotoxins
proteins excreted by the bacterial cells
Exoantigens or exotoxins
glomerulonephritis and acute rheumatic fever
streptolysin O
deoxyribonuclease B (DNase B)
Hyaluronidase
nicotinamide adenine dinucleotidase (NADase)
Streptokinase
Serological
Because the organism is unlikely to be present in the
pharynx or on the skin at the time symptoms appear
more than 20 exotoxins
documentation of nonsuppurative disease
age of onset
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Immuno PPT Flashcards Unit 3
The antibody response to streptococcal
products is variable due to what factor?
The antibody response to streptococcal
products is variable due to what factor?
What is one of the most diagnostically
important antibody?
What is one of the most diagnostically
important antibody?
What is one of the most diagnostically
important antibody?
What is one of the most diagnostically
important antibody?
Assays for detection of antibodies can be
performed individually or by using what
kit?
Streptozyme kit is useful because
The onset of clinical symptoms of
rheumatic fever or glomerulonephritis
typically coincides with what?
What is considered significant if acute
and convalescent phase sera are tested in
parallel?
Why using of at least two tests for
antibodies to different exotoxins is
recommended?
The most commonly used tests are
Antihyaluronidase tests are available for
Presence of what factor does indicate
recent streptococcal infection in patients
suspected of having acute rheumatic
fever or poststreptococcal
glomerulonephritis?
The classic hemolytic method for
determining what factor was the first test
developed to measure streptococcal
antibodies?
What test is based on the ability of
patient antibodies to neutralize the
hemolytic activity of streptolysin O?
What standard is used when ASO titer is
expressed in Todd units?
What standard is used when ASO titer is
expressed in international units?
The ASO titer may be expressed in what
unit?
The ASO titer may be expressed in what
site of infection
timeliness of antibiotic treatment
antistreptolysin O (ASO)
anti-DNase B
anti-NADase
antihyaluronidase
Streptozyme kit
detects antibodies to all streptococcal products
with the peak of antibody response
fourfold rise in titer
because production of detectable ASO does not occur
in all patients
antistreptolysin O (ASO) and anti-DNase B
research or reference laboratories
antibodies to streptolysin O
the ASO titer
The classic hemolytic method for determining the
ASO titer
streptolysin reagent
the WHO international standard
Todd unit
International unit
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Immuno PPT Flashcards Unit 3
unit?
The range of expected normal values of
ASO titer is depends on what?
The range of expected normal values of
ASO titer is depends on what?
The range of expected normal values of
ASO titer is depends on what?
Single ASO titer is considered to be
moderately elevated if the titer is
Single ASO titer is considered to be
moderately elevated if the titer is
ASO testing is currently more commonly
performed by what method?
When do ASO titers typically increase?
When is the peak of ASO titer?
Testing for the presence of what factor is
clinically useful in patients suspected of
having glomerulonephritis preceded by
streptococcal skin infections?
What factors are not stimulated in
patients with glomerulonephritis
preceded by streptococcal skin
infections?
What factors are detected in patients with
acute rheumatic fever who have a
negative ASO test result?
Why testing for anti-DNase B is highly
specific for group A streptococcal
sequelae?
What method has been developed for
anti-DNase testing?
What method has been developed for
anti-DNase testing?
What method has been developed for
anti-DNase testing?
What method has been developed for
anti-DNase testing?
The classic test for the measurement of
anti-DNase B activity is based on what?
Presence of DNase is measured by its
effect on what factor?
If a DNA-methyl conjugate is intact,
what color does it retain?
A green color intensity of between 2+
and 4+ are demonstrating
What is normal anti-DNase B titers for
patient’s age
the geographic location
the season of the year
at least 240 Todd units in an adult
at least 320 Todd units in a child
nephelometric
within 1 to 2 weeks after infection
between 3 to 6 weeks following the initial symptoms
anti-DNase B
ASO antibodies
antibodies to DNase B
DNase B is mainly produced by group A streptococci
Macrotiter
microtiter
EIA
nephelometric methods
a neutralization methodology
a DNA-methyl green conjugate
Green
Positive result
240 to 640 units
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Immuno PPT Flashcards Unit 3
children between the ages of 2 and 12
years?
What test can be used for rapid
quantitation of anti-DNase B?
What is a slide agglutination screening
test for the detection of antibodies to
several streptococcal antigens?
In Streptozyme test what are coated with
streptolysin, streptokinase,
hyaluronidase, DNase, and NADase?
What does sheep red blood cells coated
with streptolysin, streptokinase,
hyaluronidase, DNase, and NADase for?
What test is rapid and simple to perform,
but less reproducible?
In what test more false positives and
false negatives have been reported?
What titrations are performed at weekly
or biweekly intervals following the onset
of symptoms in Streptozyme testing?
What is a gram-negative,
microaerophilic spiral bacterium, cause
of both gastric and duodenal ulcers?
What method is used to determine
presence of the H. pylori?
Endoscopy used to determine presence
of H. pylori include:
Endoscopy used to determine presence
of H. pylori include:
Endoscopy used to determine presence
of H. pylori include:
The most specific test to detect H. pylori
infection is
The sensitivity of culture test is usually
lower than other methods because:
Procedures that do not require the use of
endoscopy include:
Procedures that do not require the use of
endoscopy include:
Procedures that do not require the use of
endoscopy include:
Procedures that do not require the use of
endoscopy include:
What is the primary screening method of
determining infection with H. pylori?
Infections from H. pylori result in what
Nephelometry
The Streptozyme test
sheep red blood cells
antibodies to any of the streptococcal antigens can be
detected
Streptozyme test
Streptozyme test
Several titrations
Helicobacter pylori
Stomach endoscopy
histologic examination of gastric biopsy tissue
urease biopsy test
some molecular assays
Culture
H. pylori is not evenly distributed throughout the
tissue
urea breath testing
enzyme immunoassays for bacterial antigens in the
feces
molecular tests for H. pylori DNA
antibody tests
Serological testing
IgG, IgA, and IgM
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Immuno PPT Flashcards Unit 3
antibodies production?
The presence of antibody in the blood of
an untreated patient indicates what?
The presence of antibody in the blood of
an untreated patient indicates an active
infection because:
In treated individuals, how is changed
the antibody concentrations after about 6
months?
If treatment considered successful, how
is changed the concentration of
antibody?
What is the most serological test in
clinical use of detection H. pylori?
Testing for presence of what antibody
does lack clinical value, since most
infections have become chronic before
diagnosis?
Measurement of the antibodies may be
done by what technique?
Measurement of the antibodies may be
done by what technique?
What is used in rapid test of
measurement antibodies?
What is used in rapid test of
measurement antibodies?
What technique is reliable and accurate
for the detection of H. pylori antibodies?
Tests employing antigens from a pooled
extract from what strain yield the best
sensitivity?
Why do tests employing antigens from a
pooled extract from multiple and
genetically diverse strains yield the best
sensitivity?
Most patients produce antibodies against
what proteins?
What is indicating a severe case of
gastritis or gastric carcinoma?
What is a member of a unique group of
organisms that belong to the class
Mollicutes?
What organisms do lack cell walls and
have complex growth requirements?
What does make culture of Mycoplasma
organisms difficult and time-consuming?
an active infection
the bacterium does not spontaneously clear
Decrease about 50 percent
A decrease of more than 25 percent
H. pylori–specific antibodies of the IgG class
IgM antibody
ELISA
Immunoblot
latex agglutination
flow-through membrane-based enzyme
immunoassay.
ELISA technique
from multiple and genetically diverse strains
H. pylori is heterogeneous
CagA and VacA proteins
antibodies against the CagA and VacA proteins
Mycoplasma
Mycoplasma
lack cell walls and complex growth requirements
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Immuno PPT Flashcards Unit 3
What difficulties can occur in culture of
Mycoplasma?
What infection are found in all age
groups and can often spread through
households?
What infection have following
symptoms: sore throat, chills,
hoarseness, tracheobronchitis, and
headache
What infection may remain in the
respiratory tract for several months,
causing chronic inflammation?
Laboratory diagnosis of Mycoplasma
pneumoniae involved testing for what
factor that are present in about 50
percent of patients with the infection?
What are autoantibodies that react with
the I/i antigens on red blood cells and
cause their agglutination at temperatures
below 37°C?
Testing for presence of what factor is no
longer recommended for the detection of
M. pneumoniae infections?
In what diseases cold agglutinins are also
produced?
What M. pneumoniae–specific
serological tests have been developed?
What M. pneumoniae–specific
serological tests have been developed?
What M. pneumoniae–specific
serological tests have been developed?
What M. pneumoniae–specific
serological tests have been developed?
What antibodies to M. pneumoniae may
be detected by M. pneumoniae–specific
serological tests?
What tests are the most widely used
method of detection M. pneumonia?
What test do require a small sample
volume and can test large numbers of
specimens in an automated format?
It is better to test for the presence of
what antibodies for greater accuracy, but
separately?
What test can also detect IgM or IgG
classes of antibody to M. pneumonia?
growth may take several weeks and requires
specialized media
Mycoplasma pneumoniae infections
Mycoplasma pneumoniae infection
Mycoplasma pneumoniae infection
cold agglutinins
cold agglutinins
cold agglutinins
some viral infections and collagen vascular diseases
enzyme immunoassay
particle agglutination
indirect immunofluorescence
complement fixation
IgM, IgG, and IgA
EIA
EIA
IgG and IgM
The slide-based indirect fluorescent assay (IFA)
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Immuno PPT Flashcards Unit 3
If the screening test is positive, what
should be done to quantify the amount of
antibody present?
What test may be performed using throat
swabs, nasopharyngeal swabs, sputum,
fixed tissue, and cultures?
What test is obtaining rapid results, only
one specimen is required, and live
organisms are not required (the organism
is subject to rapid drying with no cell
walls)?
What are short rods, or coccobacilli,
obligate, intracellular, gram-negative
bacteria?
The genus Rickettsia is made up what
groups?
What diseases are associated with
arthropods, spend at least part of their
life cycle in an arthropod host before
being transmitted to humans?
Arthropod hosts ticks, mites, lice, and
fleas are for what diseases?
Humans are accidental hosts for
Rickettsiae except for what organism
which causes epidemic typhus?
What are the main rickettsial diseases in
the United States?
Typhus endemic is caused by:
Typhus epidemic is caused by:
Rocky Mountain spotted fever is caused
by:
What is the method of choice for
detecting rickettsial infections?
What method may be used to detect
rickettsial infections?
What method may be used to detect
rickettsial infections?
Antibodies produced in patients with
rickettsial infections were detected by an
agglutination test known as what test?
Weil-Felix test was based on what?
Weil-Felix test was based on crossreactivity of the patient’s antibodies with
polysaccharide antigens present on the
OX-19 and OX-2 strains of __________
and the OX-K strain of____________:
serial dilution
PCR testing for Mycoplasma
PCR testing for Mycoplasma
Rickettsiae
the spotted fever group (SFG) and the typhus group
(TG)
Rickettsial diseases
Rickettsial diseases
Rickettsia prowazekii
Typhus (endemic and epidemic) and Rocky
Mountain spotted fever
R. typhi
R. felis
R. rickettsii
Serodiagnosis
probe-based immunoassays
agglutination assays
Weil-Felix test
cross-reactivity
Proteus vulgaris
Proteus mirabilis
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Immuno PPT Flashcards Unit 3
What is the one of organism-specific
serological assay for rickettsial
antibodies?
What is the one of organism-specific
serological assay for rickettsial
antibodies?
What is the one of organism-specific
serological assay for rickettsial
antibodies?
What is the one of organism-specific
serological assay for rickettsial
antibodies?
What is the one of organism-specific
serological assay for rickettsial
antibodies?
What tests are currently considered the
gold standard for detecting rickettsial
antibodies?
Testing by what methods can detect
significant titers of antibodies in Rocky
Mountain spotted fever by the second
week of infection?
Testing by IFA and micro-IF can detect
titers of antibodies in Rocky Mountain
spotted fever by when?
Antirickettsial treatment needs to be
started by what day of illness in order to
be successful?
indirect fluorescent assays (IFA)
microimmunofluorescent assays (micro-IF)
immunoperoxidase assays (IPA)
ELISA
immunoblot assays (IBA)
IFA and micro-IF
IFA and micro-IF
by the second week of infection
By the fifth day of infection
64