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immunology
exam 6
| Question | Answer |
|---|---|
| central tolerance | self eactive clones are eliminated. negative selection |
| what cell type is managed when self reactive | T regulatory cells |
| How are self reactive cells eliminated | apoptosis, anergy |
| anergy | lack of co stimulation |
| are B or T cells harder to induce tolerance in | B cells |
| What happens to self reactive T cells | the clones are eliminated |
| What happens to self reactive B cells | they aren't co stimulated |
| How can maternal AB interfere with vaccines | by binding antigen and blocking Fc receptors on B cells |
| Types of T reg cells | CD4+. CD25+, FoxP3+ |
| T reg cell function | inhibit cells via direct contact and through production of inhibitory cytokines |
| CTLA-4 | CD152. ligand on lymphocytes that T reg cells can recognize and bind to. |
| Binding CD152 does what | inhibits T cell function. |
| Is CD152 excitiatory or inhibitory | Inhibitory cell surface protein |
| What do T reg cells secrete | IL-10 and Tgf-b. Both have inhibitory effects |
| Immune priviledged sites | CNS, ocular, testes, brain |
| Maternal immune components | High progesterone, increased complement inhibitors, TH2 predominates |
| Fetal immune components | decreased complement, decreased MHC1, TH2 predominates |
| Neonatal immunity | innate and passive |
| what role does progesterone have on neonatal immunity and maternal | high levels near trophoblast (immunosuppressive) blocks lymphoid activation. lower at peripheral levels inadequate to supress systemic immunity |
| how does increased complement help neonatal and maternal immunity | block activation and complement mediated cytolysis on fetal/placental tissues. |
| why does a TH2 response dominate in neonatal immunity | humoral response. lower chance of TH1 mediated cytolysis of fetal tissue |
| at what point in gestation does lymphoid development occur | 1-5 months. |
| adaptive immune system in neonates | limited AB and T cell diversity b/c of lack of antigen. No memory cells. reduced cytokine stim to promote expansion, affinity maturation, etc. |
| at what point in gestation does phagocytic activity of neutrophils and macrophages development occur | first 3 months |
| epitheliochorial placental absorption | swine, horse. No loss, diffuse placenta. |
| syndesmochorial placental absorption | ruminants. maternal epithelial modified/fused by not lost |
| endotheliochrial placental absorption | dogs, cats. partial Ig transfer |
| Hemochorial placental absorption | primates, rabbits, guinea pigs. complete Ig transfer. AB can not pass through multiple epithelial barriers |
| what maternal placenta lining must be absorbed for Ig to pass to fetus | maternal endometrial lining |
| colostrum | milk produced late in gestation and early post partum that is highly in antibody content. IgG, IgA |
| Mechanisms of AB transfer to offspring | Endocytosed into fetal cells. Only IgG. fetal Fc receptors assist in transport and protects from degradation |
| what Ig comes from colostrum | IgG. and IgA. passes through intestinal absorption |
| what Ig predominates in ruminant milk | IgG |
| what Ig predominates in non ruminant milk | IgA |
| what percent of lymphocytes is found in colostrum | 70-80% T cells in cows. |
| causes of failure of passive immunity | 1. production failure- maternal 2. ingestion failure- placental or neonatal 3. absorption failure- neonatal |
| < 400 mg/dl IgG transferred | complete failure of transfer |
| 400-800 mg/dl IgG transferred | partial failure of transfer |
| >800 mg/dl IgG transferred | complete transfer |
| avian neonate immunity | hen actively transferes IgY from serum to yolk. IgM and IgA secreted into albumin in oviduct |
| how is IgY absorbed into chicks | bloodstream |
| how is IgM and IgA absorbed into chicks | diffuse into amniotic fluid and swallowed by chick. intestine |
| isoerythrolysis | immune mediated hemolytic anemia. AB dependent Type II hypersensitivity |
| cause of isoerythrolysis | dam is re exposed to fetal antigens. mounts AB response. concentrates AB in colocstrum. Foal absorbs AB in colostrum. binds foal RBCs. leading to hemolysis |
| blood types most commonly affected by isoerythrolysis | Aa and Qa |
| how is isoerythrolysis treated | Prevention. Do NOT let foals nurse. strip colostrum and discard. nurse mare or colostral replacement. supportive care. blood transfusions |
| how is isoerythrolysis avoided | blood type sire and dam. identift mares at risk, test mares sera. test foals RBCs for agglutination with mares colostrum |
| how is isoerythrolysis diagnosed | in vitro hemolysis. Saline agglutination. blood cross matching. blood typing |
| isoerythrolysis species affects | horse and cats. humans (RH) |
| forms of innate mucosal immunity | physical barriers, clearance mechanism, microflora |
| forms of adaptive mucosal immunity | humoral and cell mediated responses generated at mucosal surfaces |
| M cells function | pick up antigen from intestinal lumen. transported to basal membrane of APC preocessing. |
| what type of Ig is secreted for mucosal immunity | IgA |
| function of secretory of IgA | binds poly Ig receptor on basal membrane of enterocytes. eliminate or inactivate toxins within lamina propria or enterocyte. |
| intraepithelial lymphocytes (IELs) | CD8-, CD4-, gamma/delta cells. can react directly to antigen. stressed/infected cells express MHC1b. |
| IELs express what | IFN gamma. induce apoptosis |
| what layer of the intestine are most lymphocytes found | lamina propria |
| Passive vaccines | transfusion or absorption of immunoglobulins. transfer cell mediated immunity. immediate protection. good protection against weak immunogens. may transfer disease. short lived protection |
| active vaccines: non infectious agents | may contain inactivated whole or partial or recombinant particles.typically stable for long terms.safe in immuno compromised or pregnant. Th2 CD4+ response. Need lots of antigen. Need adjuvant. multiple inoculation. no memory |
| why do non infectious agent and DNA based agents s need an adjuvant | weakly immunogenic |
| active vaccines: infectious agents | modified live, attenuated, genetically engineered. single inoculation may be protective. less antigen needed. given by natural infectious route.shorter storage span, memory cells. stim TH1, TH2, may revert to virulence. not safe in immunocompromised |
| active vaccines: DNA based agents | not truly infectious b/c must be injected into cells. weakly immunogenic. require multiple innoculations,moderate antigen mass needed. need adjuvant. trigger TH1 and TH2 response. safe in immunocompromised. no vaccine shedding. |
| things needed to design a vaccine | 1. select infectious vs non- 2.select route to sim appropriate protection immunity 3.select appropriate epitope of target to vaccinate against |
| Th17 cells | confer protection against EC bacteria and fungi. trigger inflammation. |
| type 1 interferons | produced in reponse to bacterial PAMPs, boost macrophage responses enhancing production of IFNgamma, NO, and TNFalpha |
| function of type 1 interferons | reduce inflammation, active macrophages, mobilize NK cells. |
| how to type 1 interferons hinder microorganisms ability to reproduce | 1. viral infected cells secrete IFNa 2. IFNs entering neighboring cells 3. neighboring cells produce antiviral proteins that block viral reproduction |
| NKG2D expression | activation of NK cells. activated NK cells produce a large amount of IFNgamma that activate both macrophages and DCs. |
| Adaptive immunity to bacteria | 1. neutralization of toxins or enzymes by AB 2. killing of bacteria by the classical complement pathway 3.opsonization 4. destruction of intracellular bacteria by activated macrophages 5. killing of bacteria by cyto T cells and NK cells |
| heat shock proteins | highly antigenic: 1. produced in abundance during infection 2. readily processed by APCs 3. induce many cells of immune system |
| types of fungal infection | 1. affect skin or other surfaces 2. respiratory infections 3. secondary infections by opportunistic fungi |
| neutrophil activation during fungal infections | IL-23/IL-17. activate adaptive immune response. both TH1 and TH2 that enhance pro inflammatory reactions |
| adsorption | virus binds to receptors on cells |
| innate immune response to viruses | induction of type 1 interferons and activation of NK cells |
| adaptive immune response to viruses | generate of cytotoxic T cells and neutralizing AB. long term protection against virus |
| type 1 interferons | produced by the cell of innate immune system and by infected cells. |
| when do cells being to produce interferons | when they detect components of viral replication within them |
| synthesis of double strand RNA dependent protein kinase | inactivates translation of eIF2a. results in inhibition of all protein synthesis |
| activation of latent cellular endonuclease | IFN signaling induced expression of 2'5'OAS. activates a latent cellular ribonuclease (RNase L). degrades mRNA and ribosomal RNA |
| production of Mx proteins | expressed in hepatocytes and endothelial cells inhibit viral transcription and assembly of a range of RNA viruses |
| at what stage of viral infection is AB immunity effective | EX stage. before they enter host cell. IgG |
| examples of AB mediated immunity in viruses | 1. lysis (MAC) 2. Opsonization 3. phagocytosis |
| how to CTLs kill virus infected cells | release of perforin and granzymes |
| perforin | pore forming proteins |
| bacterial interference with TLR signaling | 1. weak stimulators 2.mimic receptors. cause accelerated degradation of an adaptor protein. blocks pathway 3.Suppress NFkB 4.redirect to either proinflammatory cytokines/ anti-inflammatory |
| ability to resist antibacterial proteins | 1. neutralize defensins 2. destroys cathelicidins 3. decrease defensin activity 4. blocks B defensin expression by airway epithelial cells |
| why do RNA viruses rely on antigenic variation | small genome. no room to accommodate genes dedicated to suppressing immunity. their proteins are multifunctional. |
| why do DNA viruses rely on immunoregulatory genes | have larger genomes and can afford to devote many different genes to immune evasion. |
| how do viruses evade NK cells | decrease expression of stress related proteins MICB |
| antigenic drift | gradual change in the antigenicity of a virus as a result of mutations and selection. ex : Parvo from cat to dog |
| antigenic shift | sudden, major genetic change in which a new stain develops as a result of recombination b/w 2 virus strains |
| hypersensitivity | a state of altered reactivity in which the body reacts with an exaggerated immune response to what is perceived as a foreign substance. excessive or aberrant immune response |
| type 1 hypersensitivity | form of acute inflammation. result form the interaction of antigens with mast cell bound IgE. immediate hypersensitivity |
| two important features of type 1 hypersensitivity | 1.exaggerated Th2 response 2. excessive IgE production |
| Atopy | excessive production of IgE |
| role of IL-4 in IgE induction | produced by Th2 cells. promotes dev of more Th2 cells. major source of cytokine and promote more IgE. |
| Cross linking of 2 bound IgE causes what | 1. cytokine syn and secretion 2. granule exocytosis 3. prostaglandin and leukotriene syn |
| Type II hypersensitivity | IgG or IgM mediate cytotoxic hypersensisitivity |
| what 4 conditions must occur for HDN | 1.fetus must inherit a red cell antigen from its sire that is not in mother 2. the mother sensitized to antigen 3. mothers response must be boosted by transplacental hemmorrhage or repeated pregnancies 4. newborn animal must ingest colostrum |
| when does Type III hypersensitivity develop | when antigens and AB combine to form immune complexes. if they are deposited in large amounts in tissues, trigger severe inflammation |
| what is the prerequisite for the development of immune complex disease | the persistent presence of soluble antigen and AB |
| Where do insoluble immune complexes become trapped | on the basement membrane of sm blood vessels |
| what are the most frequently affected Type III hypersensitivity sites | skin, lungs, kidney, joints, brain. where capillary beds exist |
| how long after exposure does a Type III hypersensitivity reaction occur | 6-8 hr after exposure |
| What complement pathway is initiated in Type III hypersensitivity | classical pathway. generates chemotactic peptides that attract neutrophils |
| What is the overall result of Type III hypersensitivity | Healing |
| localized type III hypersensitivity | immune complexes are deposited in tissues. rxn seen at site of antigen entry. immune complexes stay localized |
| generalized or systemic type III hypersensitivity | excess antigen in the circulation. IgG binds to circulating antigen and forms immune complexes. They circulate and get deposited in blood filtration points. sensitized individual |
| Arthus Rxn | local type III hypersensitivity. acute inflammation will develop at the injection site within 1-2 hrs. red edematous swelling. |
| what is the result of an Arthus rxn | local hemorrhage and thrombosis. if severe get local necrotic tissue destruction |
| Blue Eye | natural infection with canine adenovirus type 1 or vaccination with the live mod virus. diffuse clouding of the cornea and opacity with anterior uveitis. endothelial corneal damage. dev 1-3 wks after onset of infection |
| hypersensitivity pneumonitis | occurs in lungs when animals inhale antigen. Saccharopolyspora rectivirgula. 5-10 hrs after exposure. |
| factors that influence deposition of immune complexes | 1. size and amount of circulating immune complex 2. ability of the host to clear the immune complex from circulation 3.anatomic and hemodynamic factors determine where complexes are deposited |
| common location of complex deposition | filtration points. blood vessels. glomeruli. synovia. choroid plexus |
| Acute serum sickness | large amount of passively administered serum from a diff sp (anti-toxin). rxn occurs 10 days later. generalized visculitis with erythema, edema, urticaria, neutropenia, LN, enlargement, joint swelling, proteinuria |
| what type of hypersensitivity is seen with penicillin | all 4 types |
| glomerulonephritis | when immune complexes deposit in glomeruli. cause basement mem thickening and stim glomerular cells to proliferate |
| lesions found with glomerulonephritis | membrano-proliferative glomerulonephritis |
| what is it called when immune complexes are deposited only in the mesangium | mesangio-proliferative glomerulonephritis |
| mesangio-proliferative glomerulonephritis result | capillary endithelial proliferation, mesangial proliferation, capillary wall thickening |
Created by:
ejohnson17
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