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Veterinary Immunology '13 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Hypersensitivity

A

deleterious effects of the immune response

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2
Q

Immediate hypersensitivity

A

reactions in the humoral branch initiated by antibody or antigen-antibody complex

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3
Q

Delayed-type hypersensitivity

A

Reactions in the cell-mediated branch initiated by specific T cells

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4
Q

What is the immune reactant for Type I hypersensitivity? Type II? Type III? Type IV?

A

Type I: IgE
Type II: Ig G
Type III: Ig G
Type IV: TH1, TH2, and CTL cells

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5
Q

What is the antigen for Type I hypersensitivity reactions?

A

Type I: Soluble antigen
Type II: Cell or matrix-associated antigen; cell surface receptor
Type III: soluble antigen
Type IV: soluble antigen (TH1, TH2) and cell-associated antigen (CTL)

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6
Q

What is the effector mechanism for Type I hypersensitivity? Type II? Type III? Type IV?

A

Type I: mast-cell activation
Type II: complement, FcR+ cells (phagocytes, NK cells), antibody alters signaling
Type III: complement, phagocytes
Type IV: Macrophage (TH1), IgE production, eosinophil activation, mastocytosis (TH2), and cytotoxicity (CTL)

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7
Q

What is an example of a Type I hypersensitivity reaction? Type II? Type III? Type IV?

A

Type I: allergic rhinitis, asthma, systemic anaphylaxis
Type II: some drug allergies (penicillin), chronic urticaria
Type III: serum sickness, arthus reaction
Type IV: contact dermatitis, tuberculin reaction, chronic asthma, chronic allergic rhinitis, contact dermatitis

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8
Q

Type I hypersensitivity (hyps.) is induced by __. Explain the mechanism.

A

Allergens: induces humoral response (the plasma cells secrete IgE) –> allergens bind the Fc receptor on mast cells and basophils, they become sensitized, exposure to the same allergen cross-links the membrane-bound IgE causing degranulation, which releases mediators (systemic or localized)

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9
Q

Allergen

A

nonparasitic antigens that stimulate IgE

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10
Q

IgE is stable for weeks after what occurs?

A

it must be bound to mast cells/basophils by binding of Fc(epsilon)RI

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11
Q

Basophils are __% of circulating white blood cells.

A

1%

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12
Q

Where are mast cells found?

A

connective tissue

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13
Q

Where do most Type I Hyps. reactions occur?

A

in the mucous membranes

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14
Q

What are the high affinity Fc receptors for IgE?

A

Fc(epsilon)RI - alpha, beta, 2 gamma chains; immunoglobulin superfamily; produce and activating signal

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15
Q

What are the low affinity Fc receptors for IgE?

A

Fc(epsilon)RII; regulates intensity of IgE response

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16
Q

Describe the process of degranulation.

A

The allergen cross-links the receptor bound IgE on the surface of the mast/basophil. Enzymes (tyr kinases) are activated leading to the phosphorylation of the gamma chain and beta chain. Calcium influx then results in the formation of arachidonic acid which can be converted to prostaglandins and leukotrienes; also microtubules assembled, microfilaments contract and the granules move to the plasma membrane

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17
Q

What are the primary mediators in degranulation? When are they produced?

A

Produced before degranulation: histamine, protease, eosinophil chemotactic factor, neutrophil chemotactic factor, heparin

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18
Q

What is the function of histamine?

A

binds receptor on target cell; contraction of smooth muscle, increases vascular permeability, increase mucus secretion, stimulation of exocrine glands

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19
Q

What are the secondary mediators of degranulation? When are they produced?

A

Synthesized after target cell action: platelet-activating factors prostaglandins, bradykinin, leukotrienes, cytokines (IL-4, 5, 6; TNF-alpha)

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20
Q

What is the function of leukotrienes and prostaglandins?

A

bronchoconstrict, increased vascular permeability, mucus production

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21
Q

Systemic anaphylaxis?

A

massive release of mediators; bronchoconstriction (dyspnea, asphyxiation), smooth contract (diarrhea, urination) vasodilation (shock)

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22
Q

Localized anaphylaxis?

A

limited to specific tissue/organ; examples: atopy, allergic rhinitis, asthma, food allergies, dermatitis

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23
Q

What plays a role in the late phase (~4-6 hours following the initial reaction) that releases mediators which furthers the tissue damage?

A

neutrophils, eosinophils, macrophage

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24
Q

How do you detect Type I Hyps. reactions?

A

Skin testing: wheal and flare from local reaction

Serologic testing: RAST (radioallergosorbent test)

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25
Q

Wheal and flare?

A

The characteristic immediate reaction to an injected allergen in a skin test, in which an irregular blanched wheal appears, surrounded by an area of redness

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26
Q

RAST?

A

count the number of anti-IgE bound to allergen

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27
Q

What is the method of therapy for Type I Hyps.?

A

avoid contact; hyposensitization, induction of anergy; medications (antihistamines-bind receptor; other drugs like epinephrine)

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28
Q

Hyposensitization?

A

repeated injections of increasing doses –> shifts to IgG –> blocks allergen from IgE

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29
Q

What occurs in Type II Hyps. reactions?

A

(antibody mediated cytotoxic hypersensitivity); antibody is produced and mediates destruction

30
Q

What are the problems associated with Type II Hyps.?

A
  1. transfusion reaction: massive intravascular hemolysis of transfused RBC by antibody and complement, prevented by cross-matching
  2. Hemolytic disease of newborn: maternal antibodies specific for fetal blood group antigens cross the placenta and destroy fetal RBC’s
  3. Drug-induced hemolytic anemia: certain antibiotics adsorb nonspecifically to RBC’s –> induce antibodie –> complement lysis
31
Q

What occurs during Type III Hyps.?

A

(immune complex-mediated hypersensitivity): in some cases, large amounts of complexes form, can lead to tissue destruction magnitude depends on quantity and distribution; complement activated (C3a, 4a, 5a cause localized mast cell degranulation which leads to increased vascular permeability; C3a, 5a, 5b67 chemotactic for neutrophils leads to release of lytic enzymes and the formation of microthrombi)

32
Q

What is the difference between a localized and generalized Type III Hyps. reaction?

A

Localized: antigen injected intradermally or subcutaneously into animal with circulating antibodies –> arthus reaction (swelling, redness, eg insect bite)
Generalized: antigen enters blood stream leading to circulating complexes (serum sickness, seen with SLE, rheumatoid arthritis, lesions depend on where deposition occurs

33
Q

What occurs during Type IV Hyps. reactions?

A

(delayed-type hypersensitivity); characterized by large influx of inflammatory cells, especially macrophage; not always detrimental (important for elimination of some IC pathogens); requires initial sensitization phase of 1-2 weeks following first contact with the antigen (TH cells are activated and clonally expanded by antigen with MHCII on APC; langerhans, macrophages often the APC; mainly TH1 cells)

34
Q

What does second contact induce in Type IV Hyps. reactions?

A

Induces the effector phase: TDTH secrete cytokines responsible for recruitment and act of macrophages and others (antigen-nonspecific), reaction follows ~24 hours after 2nd exposure, peaks at 48-72 hours

35
Q

How do granulomas form in Type IV Hyps. reactions?

A

blood monocytes attracted –> macrophage –> pathogen cleaved; if the antigen is not easily cleaved -> prolonged DTH -> granuloma (can lead to extensive tissue damage)

36
Q

What would you see on histology of Type I, III, and IV Hyps. reactions?

A

Type I: vasodilation, edema, degranulated mast cells, eosinophils
Type III: acute inflammation, many neutrophils
Type IV: mononuclear cell infiltration

37
Q

Describe the immunity of the fetus and neonate.

A

The thymus develops first, followed by secondary lymphoid organs; primarily in the second trimester. The fetus is less able to combat infection than an adult…so pathogens that might not cause significant disease in the dam can be lethal to the fetus, depending on the stage of gestation.

38
Q

What is the transfer of immunity from mother to offspring dependent on?

A

type of placentation (hemochorial, endotheliochorial, syndesmochorial, epitheliochorial)

39
Q

Hemochorial transplantation

A

(primates) maternal blood in direct contact with trophoblast; IgG transferred to fetus

40
Q

Endotheliochorial transplantation

A

(dogs, cats) chorionic epithelium is in contact with endothelium of maternal capillaries; ~ 5-10% of IgG can be transferred

41
Q

Syndesmochorial transplantation

A

(ruminants) chorionic epithelium in contact with uterine tissue; NO Ig across placenta

42
Q

Epitheliochorial transplantation

A

(horses, pigs) chorionic epithelium in contact with the uterine epithelium; NO Ig across placenta

43
Q

What is colostrum rich in and why is it important?

A

rich in IgG, IgA, IgM, IgE, (IgG most important); most of the immunoglobulin is serum-derived; proteolytic action of GI tract in neonates is low –> colostal protein –> reaches intestines –> bind Fc rec on GI epithelium –> pinocytosis of immunoglobulin –> eventually reach circulation

44
Q

In the horse and pig, which immunoglobulins are preferentially absorbed?

A

IgG and IgM

ruminants: unselective

45
Q

When is permeability of immunoglobulins in colostrum highest?

A

after birth

46
Q

When does the secretion of immunoglobulins change to milk?

A

gradually - milk rich in IgG1 and IgA in ruminants and IgA in nonruminants (helps protect against enteric infection)

47
Q

What are the 3 reasons for failure of passive transfer?

A
  1. production failure - can be seen in premature births or premature lactation
  2. ingestion failure - multiple births, poor mothering, poor suckling drive, weak offspring, congenital defects
  3. absorption failure - intestines don’t absorb the Ig
48
Q

__ are present in colostrum and aid in the protection for ~36 hours.

A

lymphocytes

49
Q

Passively acquired __ interfere with the ability of the young to respond to vaccination.

A

antibodies

50
Q

How does passage of immunoglobulins work in the chick?

A

immunoglobulin in hen serum –> yolk -> some absorbed by chick; IgM, IgA diffuse into amniotic fluid –> ingested by chick

51
Q

What is the immunologic basis of graft rejection?

A
  1. transplantation is the transfer of cells from one site to another
  2. rejection is the immunologic reaction to grafter tissue
52
Q

What are the four graft types?

A

autograft (self tissue, same individual)
isograft (genetically identical individuals)
allograft (same species)
xenograft (different species)

53
Q

Histocompatibility

A

refers to the antigenic similarity (or dissimilarity) of two tissues [various antigens, MHC important, haplotype, minor loci-recognized in context of self MHC]

54
Q

Rejection is primarily a cell-mediated immune (CMI) response with what 2 stages?

A
  1. sensitization - T cells recognize the foreign antigen and proliferate in response (recognition of MHC and graft’s self peptide, MHCI -endogenous; MHC II -exogenous; TH interact with APC, host and donor; effectors generated - mainly TH - recognize foreign MHC II of foreign peptide in self MHC II)
  2. Effector - CMI reactions (DTH and CTL); antibody and complement less common; TC recognizes foreign MHC I; CK’s important (IL-2 for CTL’s, IFN-gamma for DTH, TNF-beta directly cytotoxic)
55
Q

Rejection can be rapid, acute, or chronic. Describe each.

A

Rapid rejection due to pre-existing antibodies.
Acute mediated by TH and macrophages.
Chronic involves humoral and CMI

56
Q

Describe blood groups.

A

RBCs have surface antigens that can lead to reactions which leads to intra- and extravascular hemolysis. Antibodies agglutinate and mediate hemolysis and opsonize.

57
Q

How can you prevent severe reactions from occurring with transfusions?

A

by cross-matching: donor cells with recipient serum (major) and donor serum with recipient cells (minor)

58
Q

Hemolytic disease of newborns

A

leakage of fetal blood cells into maternal circulation will generate an immune response by the dam; the resultant antibodies ingested in colostrums by newborn lead to hemolytic disease

59
Q

Blood groups of cattle? sheep? pigs? horses? dogs? cats?

A

Cattle: 11; B and J most important
Sheep: 7; B and R most important
Pigs: 15; A most important
Horses: 7; hemolytic disease of newborns more common with foals, esp. mules; anti-Aa more severe; Qa less severe; anti-R and Anti-S mild; Mares negative for Aa or Qa are most likely to hae affected foals
Dogs: 11; only A is clinically significant; ~60% are A+
Cats: one major blood group, AB; ~75-95% are A+, ~5-25% B+, <1% AB; CROSS MATCHING ESSENTIAL…otherwise acute shock results

60
Q

virus

A

nucleic acid, protein, lipid with glycoprotein

61
Q

describe the non-immunologic resistance of viruses.

A
  1. interferon- stimulates production of proteins with antiviral activity (IFN-alpha, IFN-beta, IFN-gamma); produced by infected cell, released, bind cell receptor on adjacent cells to induce “antiviral state”; blocks virus transcription; interferes with virus replication at several levels; enhances the immune response
  2. innate resistance = physical barriers, enzymes, phagocytes
62
Q

IFN-alpha is produced by _.

A

WBCs

63
Q

IFN-beta is produced by __

A

fibroblasts, epithelial cells

64
Q

IFN-gamma is produced by __.

A

T cells, NK cells

65
Q

Describe the evasion of viruses.

A

mutations; non-neutralizing or slow response or AB; “hiding” (e.g. latency); induction of tolerance

66
Q

Bacteria

A
  1. innate resistance - physical barrier, enzymes, lactoferrin, complement
  2. antibodies - neutralize toxins; opsonization; complement activation
  3. macrophages, neutrophils - phagocytosis
  4. CMI for IC bacteria
67
Q

Describe the evasion of bacteria.

A

capsule, inhibition of opsonization, phagocyte depression, inhibition of chemotaxis, toxins, proteins that mask Fc, proteins that inhibit respiratory burst, proteases

68
Q

What are the 2 types of parasites?

A
  1. protozoa

2. helminths

69
Q

Describe protozoa.

A

Macrophage - phagocytosis; antibodies - opsonize, agglutinate, immobilize, complement activation, ADCC; CMI - Tc important with these IC pathogens; Evasion - may induce immunosuppression; some become nonantigenic; alter surface antigens

70
Q

Describe helminths.

A
  1. antibody - IgE induces local type I reaction
  2. Macrophage, platelets, eosinophils have receptor for IgE
  3. Eosinophils degranulate at site
  4. other antibodies may neutralize parasite
  5. CMI in some
  6. Evasion - decreased antigenicity; expression of host antigens; antigenic variation; interference with antigen presentation; block macrophage proteases, degrade immunoglobulin, inhibit chemotaxis
71
Q

Difference between primary and secondary immunodeficiency.

A

Primary: inherited disorders
Secondary: due to extrinsic causes; immunosuppression

Veterinary Immunology '13 (5 decks)

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