Immuno - Midterm 2

drraythe's version from 2015-06-14 23:44


Question Answer
What is an inductive site? What occurs here?Sites where Ag are encountered, processed, & immune responses are initiated. (ex: tonsils, GALT)
What is an effector site? What occurs here?Mucosal sites where the immune responses that were initiated in the inductive site are now carried out (diffuse lymphoid tissue at mucosal surface)
Form of secretory IgA? What does it do at mucosal surface?Dimer. IT PREVENTS ADHERENCE AT MUCOSAL SURFACE (immune exclusion)
How does IgA produced by plasma cell in submucosa reach lumen?It binds to a poly-Ig-receptor which allows it to be endocytized & pass through
How can IgA act intracellularly?It can still bind to invading or infecting pathogens & neutralize them w/in the cell while it's being transported...or follow the pathogen into the cell
What is immune exclusion?When an IgA won’t let a pathogen adhere to the mucosal wall to infiltrate body
How is IgA not digested by enzymes at mucosal surface?The poly-Ig-receptor cleaves off when the IgA is in the lumen, but a small part remains called the SECRETORY PIECE which makes it resistant to enzymes
What animal species have no antibody in blood at birth?Horses & ruminants
What animal species have very little material antibody in blood at birth?Cats & dogs have very little. (Primates have a lot)
Zinc turbidity test to test? How?Test FPT (failure of passive transfer). Zinc binds to Igs & precipitates them, if the sample is clear, it's FPT
ELISA to test FPT how?Snap foal IgG (color change test) (so if testing foal, anti-equine IgG binds to any IgG in foal serum sample, then add more anti-equine IgG w/ color tag...more color = more IgG = good)
Radial immunodiffusion test for FPT how?Put foal serum in a well in a gel which has variously sizes wells next to it...over time, the size of the sample well & 1 of the other wells of corresponding amount of Ig will measure up so you know how much Ig the unknown sample has compared to the known amts
Serum protein electrophoresis for FPT how?(Same as stated previously...) Measure total proteins & how much the gamma fractions (Igs) contribute to it
How do you treat FPT?Depends on your time interval
(1) 1st 15 hrs, orally give 2-3L of good colustrum
(2) >15hr <3wk, give plasma of mom IV or IP
(3) ~3wk, watch & give antibiotics - by this time its immune system has had time to respond to antigens
Colustrum vs milk (antibody present, amount present?)Colustrum = MOSTLY IgG (60-95%) rest is others
Milk = mostly IgA (however still IgG predom in milk in rumis)
When can Ab be absorbed in newborns GUT?1st 24 HRS
What is gut closure?After 1st 24hrs, Abs can no longer (or barely) be absorbed
Why is it fine if the Ab in milk isnt absorbed bc of gut closure?Milk = IgA. IgA is DESIGNED TO WORK IN GUT LUMEN, doesnt need to be absorbed
Why dont we vaccinate young animals?Maternal Ab can interfere
Type I hypersensitivity. Speed? Cells involved? Role of IgE & allergens?ALLERGIES. Needs PRESENSITIZATION. Antigen = allergen. Immediate/fast, involves mast cells, basophils, Th2 cells. IgE antibody is used, it makes the mast cells degranulate for the inflammatory response (HISTAMINE & HEPARIN)
Type I hypersensitivity general mechanism(2⁰ response) IgE bound to surface of mast cell. Mast cell+IgE encounter antigen (allergen) & immediate degranulation of mast cell takes place while IgE binds to antigen. This causes the acute & fast inflammatory response. (1⁰ response is when APC & Th2 & B cells are involved in making the IgE to attach to the mast cell)
Localized type 1 vs systemic type 1 hypersensitivity rxn?Localized = Localized to 1 organ system. Systemic = Anaphylactic shock (vasodilation, hypotension, vascular permeability, bronchial constriction)
To diagnose type 1 hypersensitivity?(1) Skin test for a localized reaction to antigen
(2) Can measure total & specific IgE via ELISA
Treatment of type 1?(1) Epinephrine to inhibit mast cell degranulation & effects of it
(2) Antihistamines
(3) Corticosteroids
(4) Anti IgE antibody
(5) Desensitization
Type II hypersensitivity-role of antibody & complement? What kind of antibody participate?(HEMOLYTIC HYPER-SENSITIZATION) mediated by IgG/IgM. Pre-existing specific antibody binds to antigens on surface of cell can causes destruction of cell (destruction can be via complement proteins, ADCC)
Target cells of type II h.s. are?RBC'S!!! (+web’s, thrombocytes)
Mechanism of type II h.s.?Antibody mediated destruction of cells
Clinical results of type II h.s.?Anemia, Leukopenia, Thrombocytopenia
In type II h.s. what triggers Ab that then binds to the target cells? (2 kinds)(1) PREFORMED ANTIBODY = Antibody to blood group antigens (transfusion reactions!), mares colostrum (hemolytic dz of newborn)
(2) 2⁰ causes = Drugs, infectious agents such as hemoparasites
1⁰ causes of type II h.s. are ___ or ___Idiopathic or autoimmunity
3 examples of type II h.s. reactions involving RBC antigens?(1) Xfusion reaction
(2) Hemolytic dz of newborn
(3) Penicillin acting as a hapten (other drugs also)
Hemolytic dz of newborn...explain**HORSES**. Baby has dads RBC type. Mom is exposed to dad RBC type when baby is born, mom makes antibodies against it (sensitization period). Her anti-dad antibodies are produced & placed into the colostrum. 2nd baby is born, baby suckles & ingests anti-dad (baby’s blood type) antibodies, baby's immune system attacks its own RBCs bc they are marked w/ mom's anti-dad antibodies - ONLY IN 2ND BABY MOM HAS HAD
Why does hemolytic dz of newborn only happen in 2nd baby, not 1st?Mother exposed to dad RBC type at baby’s birth - colostrum only lasts 24 hours but takes mom a week or 2 to make the Ab against it. However, this Ab is present when 2nd baby born, it suckles, gets anti-self Ab, & its RBCs are lysed by its own immune system
How do you diagnose immune-mediated hemolytic anemia?Coombs test
Type III h.s. mechanism?(IMMUNE COMPLEXES)... Ab-Ag complex forms, complex deposition, complement activation, neutrophils, mast cells degranulated by complements (+/-)
(Example of) antigen that can result in immune complex formation?FIP
2 types of type III h.s.?Localized & generalized (gen = complexes formed in circulation & then deposited, usually in sm vessels)
3 examples of LOCALIZED type III?(1) Arthus rxn (inject things SQ, severe inflammatory rxn w/ complexes)
(2) Blue eye in dogs (complex against adenovirus in eye causes corneal edema & opacity)
(3) Heaves in horses (complexes in lungs from mold/dust inhaled)
3 examples of GENERALIZED type III?(1) Serum sickness (serum from another species has foreign proteins. generalized vasculitis etc ensued)
(2) Glomerulonephritis (usually caused by an immune-complex Dz, the complexes damage glom)
(3) Purpura hemorrhagica 2⁰ to step equi infection in horses (vasculitis) (not all infected horses get this)
Dx of type III h.s.?Detection of Ab in tissue via immunofluorescence
Tx of type III?Treat underlying condition, suppress immune system
Type IV h.s. mechanism?(DTH) Th1 RESPONSE! Activation of macrophages & CTLs, tissue damage
Ex of an agent that could cause a type IV response?Mycobacterium protein (TB!)
Contact hypersensitivity is for which h.s. rxn? Examples?TYPE IV. Ex) poison Ivy. (Ag binds to SKIN PROTEIN)
Antigen/consequence of DTH CONTACT h.s.?Haptens → Contact dermatitis
Treatment of contact hypersensitivity?Avoidance, Antinflammatories, Antibiotics if there is a resulting 2⁰ infxn
Type IV h.s. to transplants (what happens? 2 types?)Immune system reactions to FOREIGN MHCs
(1) Host vs graft - host immune system attack graft MHCs/cells
(2) Graft vs host - xplanted organ's immune response to the host's tissues

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