Immunology
Body defense may be:-
Non-specific resistance
specific resistance
1st line
2nd line
3rd line of defense
Skin & mucos
. Phagocytosis
Membrane
B, T lymphocytes
. Inflammation & fever
antibodies.
- Phagocytes are neutrophiles & monocytes.
- Chemotaxis is the chemical attraction of phagocytes towards the site of
infection through chemotactic factors.
- Infection increase the number of leukocytes "leukocytosis"
- Fever is the systemic response of the body to infection or injury.
- The complement system:- is a group of 20 or more proteins present in
blood.
- Complement system increase the action of antibodies in killing
microorganism.
- Classical pathway activation of complement :- Ag-Ab complex activate C1
- Alternative pathway activation of complement :Activation doesn't involve Abs but occur through polysaccharides.
- The complement system remove Ag – Ab complex from the circulation as
if Ag – Ab complex ppt in the kidney it will cause glomeruloneohritis.
- C-reactivate protein "C-RP" :- it is one of the acute phase proteins,
synthetized in liver, can activate complement system so kill m.o.
.it's a marker of inflammation. And reach its peak after 24 hour.
- Antistreptolysino "ASO": It is antibody produce by the body as defense
mech. against streptolysin which is an enzyme produced by the invading
streptococci.
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:. ASO in case of streptococci & if untreated Aso react W the heart
muscle tissue causing "rheumatic fever"
- Interferon
α, B, Ϫ
α,B
produced from the infected cells.
Ϫ
produced from T-lymphocytes.
.IFN has an antiviral activity.
.IFN is host cell specific but not virus specific as human IFN has only
activity in human but against all viruses.
When the cell is infected with a virus, the cell process the virus into small
protein fragments that move to the surface of the infected cell acting as
antigens these antigens are present in association with MHC which act as
presenters for those antigens so these antigens are well marked and highly
lighted for t-cells.
. ͘ . MHC
major histocom patibility cpx
‫ ) لكى تتعرف عليها ونقوم بقتلها‬Tc( ‫) ل‬viral parts)‫و هى تعمل مثل الصينيه لتقديم ال‬
Immunity
Naturally acquired
artificially acquired
Active
passive
Ag enter the readymade Abs pass
Blood so
freely from the mother
Body from Ab. To the baby during
Pregnancy or during
Colostrums "lactation"
active
passive
pathogen is given in ready made Ab
injection
e.g. vaccine
e.g. serum
Serology is the study of reactions between Ags and Abs.
Abs separated from serum by Gel-electrophores is
Antibody ≡ Ϫ globulin ≡ Immunoglobulin ≡ Ig.
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Antigen "Ag": material that induces production of antibodies when
injected Into the body.
Has large M.WT ≥ 10,000 Dalton. Mainly proteins or large
Polysaccharides .
Ag may be the whole bacterial cell, capsule, flagella, viral coats,
Toxins, pollen grains, dust or egg white.
Epitopes is a specific regions on Ags which the Ab recognize it and bind to it.
Haptens: - foreign substance having low M.WT it's not immunogenic,
Can't stimulate the immune system to produce Abs.
Hapten + carrier
Ag "immunogenic"
Example of haptens is penicillin.
Antibodies"Abs" are proteins made in respone to antigen
And it can recognize it and bind with it.
Most of Abs are bivalent "have 2 antigen binding site"
Ab structures
4 protein chains
2 light "L".
2 heavy "H".
Intra disulfide links bet. 2H but inter sulfide bond bet bet. H and L.
Ab has a Y shape and the lower parts of the Y shape is the constant
Region "C"
Fc region
composed of the 2 heavy chains "The lower part".
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The end of the two arms of the Y-shape are called variable
Region "V" which is the antigen binding sites.
The real form of Ab is the Y-shape structure in which the amino acid
Forming the chains exist in form of domains.
L
has 2 domains
VL and CL
H
has 4 domains
VH and 3 CH
Constant region of heavy chain has many different amino acid sequences
resulting in 5 different classes of Ig (s).
IgA, IgG, IgE, IgM, IgD.
IgM is the first Ab secreted due to initial infection.
I9G
structure
monomer
I9M
I9A
pentamer
Diamer
I9D
monomer
I9E
monomer
% of total
Abs serum
80%
5-10%
5-10%
0.2%
0.002%
Complement
fixation
Placental
transfer
yes
yes
No
No
No
Yes
No
No
No
No
location
function
Blood,
lymph, and
intestine
Blood,
Secretions
lymph, B-cell "salvia, mucus,
surfaces
milk, blood,
lymph"
phagocytosis 1 ˢᵗ Ig
Protection on
secreted
mucosal
surface
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B-cell
surface
Bound to
mast cell
Immune
responce
Allergic Rx.
Humoral immunity (Ab –mediated immunity) :Through circulating Abs W are secreted from B-cells.
B-cells activation activated B-cells differentiated into plasma cells Specific
Ab produce + Memory cells
Cell-mediated immunity: - depend on t-cells
And act against pathogen intracellular not Circulating. And fight cancer cells.
Stem cells
Produce
present in bone
Marrow in adult and
In liver of foetus.
Immature
immature
B-cells
T-cells
Maturation
maturation
In bone marrow
in thymus gland
Mature B-cell
mature t-cell.
Activation by
Ag(s) on pathogen
Activated B-cells
activated
Differentiation
cytotoxic (tc)
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Plasma cells +memory cell
form
attack cancer
cells and
Ab(s) specific for
intracellular ,
The Ag
viruses , Bacteria.
Every single B-cell can be activated only by one specific Ag
"Key and lock".
Each B-cell can bind only to one Ag using the Ag
Receptor (Igd, IgM) Which are bound to the surface of B-cell then the B-cell is
activated.
Activated B-cells
plasma cells + memory cells "Long term immunity".
The human body make 100 million lymphocytes each day so an equivalent No. of
other lymphocytes must die otherwise leukemia occur.
So Apoptosis
is a programmed cell death.
The 1ˢᵗ Ab formed IgM followed by IgG.
Experianent in rabbit.
B-cells
cancerous B-cell
cant produces Abs but contine
"Myelomas"
Hybrid cell
In
in grouth in cultne.
B-cells + myeloma fusion
selective medium
hybridoma
Produce monoclonal Ab.
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Cytokines is the chemical messengers of immune cells.
Interleukins are cytokines that serve as chemical messenger
between leuckocytes.
The cells that introduce the Ag on its surface are called "antigen presenting
cells"APC(s)".
CD4 types:- TH and TD.
Types of t-cells
CD8 types: - Tc and Ts.
TH "helper": - activate the cytotoxic T cells
Activate the macrophage
Help B-cells to produce Ab(s).
TD "delay hypersensitivity t cells": Involve in allergic reaction
Involve in rejection of transplanted tissue.
Fight intracellular Ag.
Tc "cytotoxic": - attack infected host cells and
Destroy them by secreting perforins and
Lytic enzymes.
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Ts "suppressor": - regulate the immune response by turning it off when Ag is no
longer present.
TC bind to MHC-antigen cpx on infested cell surface,
Tc release perforins W lyse cell.
Vaccines: 1-Live attenuated: - make the organism immunogenic but not pathogenic
E.g. Sabine vaccine.
2-Killed: - the organism is killed by formalin or phenol
E.g. Rabies vaccine, salk vaccines and cholera, influenza.
3-Toxoid: -toxin inactivated toxoid
E.g. tetanus and Diphtheria.
4- Subunit vaccine "recombinant vaccine".
E.g. hepatitis B.
Hypersensitivity Rx: -
Anaphylactic
cytotoxic
Type 1
type 2
immune cpx
type 3
cell-modiated
or delay type
Type 4
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1-type 1 "anaphylactic" IgE produced on the 1ˢᵗ exposure to the allergen and
attach to mast cells or basophiles so on the 2ⁿᵈ Exposure mast cell degradation
and releasing of histamine and leukotrienes and vasodilatation, mucous
secretion B.V permeability and bronchoconstriction.
E.g. pollen grains, eating fish, nuts, strawberry, Hay fever, urtecaria, asthma.
In non-allergic people, igG produced.
2- Type TT "cytotoxic": involve the activation of the complement.
E.g. blood transfusion,
Type O
lack A and B Ag(s),
Type AB
has A and B Ag (s),but lack Ab(s) to them.
Blood type O is universal donor.
And blood type AB is universal recipient.
RH factor: Father+Rh
Child +RH
mother-ve
RH
RBCs of child + Ve through to the
placenta
mother –Rh
IgG
2ⁿᵈ pregncy
IgG
Pass to the +ve
RH child
"antiRh"
hemolytic disease of newborn.
3- Type 3 which is Drug hypersensitivity.
4- Type 4 : cell mediated Rx "delayed type" TD cells are involved.
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E.g. allergic contact dermatitis soap,Gloves "latex one" Poison ivy. And
tuberculin Rx by mycobacterial Ag
Autoimmune disease
the production of Ab(s) against the persons own tissue Ag(s).
1-Graves disease: due to Ab(s) called long acting thyroid stimulators.
"TSH receptor" Ab binds to receptors on thyroid gland so thyroid hormones
amount so hyperthyroidism.
2- Myasthenia gravis: gradual loss of muscular tone caused by the Ab(s) that
Coat the Ach receptor at the NMJ "neuromuscular junction".
So the muscle controlling the diaphragm don’t receive the Nerve signals
Respiratory death.
3- Pernicious anemia: - vit B₁₂ need intrinsic factor to be absorber
And her there are Ab(s) to the intrinsic factor so vit B₁₂ can't bind to the
Intrinsic factor so Vit B₁₂ deficiency.
4- Rheumatoid arthritis: - immune cpx of IgM and IgG are deposited in joints
affect females> male.
5- Systemic lupus erythromatous (SLE): Ab(s) against DNA are formed
. ͘ . Ab-self AgDNA cpx
deposit in much tissue causing glomerulonephritis.
6- hashimotoo thyroditis :
T-cell attack thyroid gland cell and causing hypothyroidism.
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7- IDDM
t-cell attack and destroy B-cell of lengerhans.
8- Good pasture syndrome: Abs against capillary absement membrane
(GMB)
. ͘ . nephritis and these Abs may pass to the Pulmonary capillary
basement membrane causing Pulmonary hemorrhage.
9-Multiple sclerosis (MS): T-cell attack the basic protein myelin Leading to CNS
demylination with sclerotic plaque.
10-sojorin syndrome:
Abs against salivary gland antigens and exocrine glands of the eye,
GIT and RT and vagina so no exocrine gland secretion.
Autoimmune diseases
Type 2
Autoimmune
type 3
type 4
autoimmune
hashimotos
Disease
disease
thyroditis
Pernicious Anemia
SLE
IDDM
Graves's disease
Rheumatoid
Myasthenia gravis.
Arthritis
Tolerogens
cpds are broken by the body and have specific no
responsiveness.
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TTT of type 1 hypersensitivity reaction: 1-H₁ blocker.
2-EPi.
3-cromolyn Na⁺.
4-topical steroids.
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