Flashcards: Ch 16/17 test yey!

Overreactive immune system leads to reacting to things that are not a threat (allergies, autoimmune disease)

Repeat contact with antigens called allergen

Inhalants- pollen, mold spores, formalin

Ingestant- Peanut, additives, aspirin

Injectant- Hymenopteran, insect, drug, enzyme, hormone

Contactant- heavy metal, detergent, formalin, dyes

Sensitization- Dendritic cell present allergen to T helper 

-B cell activated to form plasma and IgE (immunoglobulin E)

-Fc on IgE bind to mast cell/basophil =primed Ig-E (memory cell)

-Basophil found  in blood stream and mast cell in tissue 

-No symptoms 

Provocative, Subsequent exposure

-Allergen arrive again

-attaches to IgE on mast cell and trigger degranulation -release cytokines(histamine, serotonin, prostaglandin, leukotriene, bradykinin)

-Systemic distribution of mediator in blood 

-Symptoms on skin, upper respiratory, GI, conjunctiva

rash, cough wheezing

Hay fever- Allergic rhinitis

Allergic asthma- impaired breathing and severe brochoconstriction

A topic dermatitis- eczema

wheal and flare inflammatory reaction to local injection of allergen

sudden respiratory and circulatory disruption

•Tryptase and histamine release test:  Released from mast cells and basophils during an allergic reaction. Can be done in vitro.

•Skin testing: Allergens are applied to the skin

•Treatment block pathway to an allergic reaction 

-Avoid allergens- prevent degranulation of mast cell

-Corticosteroid (plasma, no synthesized IgE)

-Cromolyn( mast cell, stop degranulation)

-Antihistamine( counter effect of cytokines, prevent effects of mediatior?)

Desensitization therapy-IgG intercept allergens before they encounter IgE

SLIT-tiny allergen under tongue

inducing the production of IgG, which act as “blocking antibodies” which intercept allergens before they encounter IgE

tiny allergen under tongue. IgG antibodies formed instead of IgE, remove allergen before reacting with mast cell 

Antibodies(IgG & IgM) bind to foreign blood, initiate the complement system, and lyse blood cells

different molecules on blood transfer/organ transplant

antigen markers on RBC made of glycoprotein

1 from each parent. 3 different Alleles, A, B, O

A blood has N acetylgalactosamine

B blood has D galactose

O has neither A or B antigen, so has both anti A and anti B antibody(universal doner)

AB has both A & B antigen, so it has neither a or b antibody(universal recipient)

contain Anti A/B antibody, used to test transfusions for agglutinatinon

Erythroblastosis fetalis

RH factor (D antigen) + Has RH allele, must be exposed 

Rh- mom is sensitized to RH+ baby. 

Another RH+ baby can cause HDN

RhoGAM(anti-RH antibody) can be given to mom during each preganacy to stop sensitization, block antibody

when antibodies combine with soluble antigens (i.e. proteins)

•Ab/Ag stuck in basement membrane

Neutrophils come and  damage tissues = immune complex reaction 

Arthus reaction- acute localized response to second vaccine/ drug

Serum sickness- systemic injury by antigen-antibody complex in blood

Occurs when T-cells and antibodies do not differentiate self/ non-self attack own antigen

Delayed Reactions-

•Mediated by Th1 cells rather than antibodies

•Effects are delayed, showing up 48-72 hours after 2nd contact with an antigen

•Contact dermatitis- Allergen, poison oak, processed by langerhan cell then next exposure= CD8 lymphocyte

•The Mantoux TB test reaction to dead tuberculosis cells indicates that T-cells sensitized to TB present

Immune system of recipient T cell recognizes class I MHC graft as foreign release IK-2.  Leads to loss of donated organ.

Graft versus Host Disease

bone marrow transplants, when WBCs from donated marrow recognize recipient as foreign, systematic peeling rash .

•Graft rejection is lessened using immunosuppressant drugs (for life)

•Cyclosporine

•Methotrexate

•Prednisone

•Autograft:  Same person (butt to face)

•Isograft:   Identical twin

•Allograft:  Same species, different people 

•Xenograft:  Different species, animal

(present at birth)

(acquired after birth)

•One or more Ig’s are reduced or absent

•Often X-linked (more common in males)

•IgA deficiency: ~1 in 600 most common

•Agammglobulinemia:  Rare, absent B cells

•Infections begin at about 6 months

•Usually more severe as T-cells control functions are lost as well as direct cell actions

•DiGeorge Syndrome (thymic aplasia) absent: 

•Absence of thymus

•Simple disease may be fatal

•Immunizations with live microbes may not be possible

-more common in males

•Severe Combined Immunodeficiencies (SCIDs)

•Lack of both stem cell lines

•Infections begin within days of birth

•E.g. Adenosine deaminase deficiency (ADA)- autosomal recessive defect in metabolism of adenosine

•Infection (HIV, Epstein-Barr virus, measles virus, Hansen’s disease (leprosy)

•Organic disease (Cancer, diabetes)

•Chemotherapy

•Radiation

•Antibodies can be used to detect specific antigens in blood, urine, cerebrospinal fluid

Agglutination, precipitation, complement fixation, fluorescent, antibody test

•Antibodies are used to detect soluble antigens (proteins)

•Typically only visible under a microscope

•Antibodies are used to detect cells

•Typically visible with the naked eye

concentration of antibody in serum by diluting

Capture or antibody sandwich ELISA)

detect the presence of an antigen (bacterial cell, virus).

Well of ELISA coated with antibodies

Antigen sandwich between 2 antibody

Unbound antibody washed away

used to detect the presence of antibodies (e.g. against Coronavirus)

•The level of antibodies in the serum is referred to as titer. 

High titer=high level of antibodies

Well of ELISA coated with antigen

Antibody used to detect other antibody

Unbound antibody washed away

Lupus (SLE)

•Rheumatoid arthritis

•Graves disease and Hashimoto’s disease

Type I Diabetes

•Myasthenia gravis

Multiple sclerosis-

rheumatic fever

•Specificity:

•Sensitivity:

common allergy and anaphylaxis

IgE, mast cell, basophil, allergic

Anaphylaxis, allergies, hay fever

IgG and IgM mediated cell damage cause cell lysis

blood group incompatibility, pernicious anemia, myasthenia gravis

immune complex diseases 

IgG deposited into basement membrane

lupus, rheumatoid arthritis, serum sickness, rheumatic fever

T cell mediated

delayed hypersensitivity and cytotoxic reaction

contact dermatitis, graft rejection

allergy that is localized to region, not life threatening. Rash asthma, coughing wheezing

allergy that is systemic, airway obstruction, chemical mediator elevated. (bee stings, peanuts, injection of antibiotics)

allergy med to stop plasma, no synthesized IgE

allergy med to stop mast cell, stop degranulation

allergy med to stop counter effect of cytokines, prevent effects of mediatior

•Autograft

•Isograft:

•Allograft:

•Xenograft: