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Immunology > exam 3 > Flashcards

exam 3 Flashcards

1
Q

possible fates of Tcells in central tolerance

A

if recognize self Ag: cell death or development of Treg cell

react below threshold: positively selected: migrate to periphery as mature T cell

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2
Q

possible fates of B cells in central tolerance

A

react with self AG with high avidity: apoptosis or BCR editing of light chain

weak recognition of self Ags: anergy

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3
Q

what conditions induce differentiation of an induced Tregulatory cell

A

Ag recognition in the presence of TGF-beta and absence of IL-6 and presence of IL-2
(induces expression of FoxP3)

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4
Q

what conditions induce differentiation of a Th17 cell

A

Ag recognition in the presence of TGF-beta and IL-6

induces expression of retinoic acid receptor (RAR) making it a Th17

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5
Q

mechanism of Bcell peripheral tolerance

A

when B cell recognizes Ag in periphery, CD22 receptor is phosphorylate by Lyn which recruits SHP-1 which blocks BCR function

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6
Q

AIRE function and deficiency

A

AIRE is a transcription factor that is associated with thymic epithelial cells displaying self Ags. without it, negative selection of Tcells is impaired (self reactive Tcells can enter circulation and cause damage to tissues)

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7
Q

CTLA-4 funciton in Tregulatory cells

A

acts as a competitive inhibitor, binds B7 on APC, blocking CD28 from binding to B7 which is a necessary co-stimulator

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8
Q

CD25+ function on Tregulatory cells

A

IL-2 receptor which is essential anti-apoptotic signal

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9
Q

define immunologic ignorance

A

T cells that are physically separated from their specific Ag and cannot become activated

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10
Q

function of CRP (C-reactive protein) and SAP (serum amyloid protein)

A

bind bacterial surfaces and to the globular heads of C1q to activate classical pathway of complement

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11
Q

differentiate between endotoxins and exotoxins produced by bacteria

A

endotoxins: components of bacterial cell wall
exotoxins: secreted by the bacteria

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12
Q

what are the innate immunity mechanisms against bacteria

A

complement activation
phagocytosis
inflammation

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13
Q

how does bacteria activate complement

A

mannonse on surface binds mannose-binding lectin –> lectin pathway

peptidoglycans in gram positive and LPS in gram negative activate alternative and classical

CRP and SAP activate classical by binding both C1q and bacterial surfaces

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14
Q

how does Factor I prevent host bystander damage

A

it cleaves C3b and C4b preventing formation of active convertase

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15
Q

what is the MAJOR mechanism used by bacteria to evade humoral immunity

A

variation of surface Ags

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16
Q

list 3 effector mechanisms of Abs (humoral adaptive immunity) against bacteria

A

toxin neutralization
opsonization
complement activation via classical pathway

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17
Q

how are NK cells activated (early and late in viral infection)

A

IFN-alpha released from epithelium early in infection

IFN-gamma and IL-2 from Th1 cells in later stages

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18
Q

costimulatory/stabilizing interactions between APC and class II MHC

A 
CD4:class II MHC
CD80/86:CD28
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19
Q

explain how NK, DCs and macrophages activate eachother inorder to degrade phagocytosed materials (bacteria)

A

activated DCs and macrophages produce IL-12 and IL-15 which activate NK cells
NK cells produce IFN-gamma which inturn promotes killing of phagocytized bacteria by macrophage

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20
Q

describe endogenous pathway of Ag presentation

A

intracellular pathogens (virus) are degraded by proteosome and peptides are shuttled to ER via TAP proteins. the peptides are then loaded on MHC class I and delivered to cell surface

21
Q

describe exogenous pathway

A

extracellular pathogens are engulfed by phagosomes. inside the phagosome the pathogen-derived peptides are loaded on MHC class II and delivered to the surface.

22
Q

define autograft

A

grafts exchanged from one part to another part of the same individual

23
Q

define isografts

A

grafts exchanged between different individuals of identical genetic constitutions (identical twins)

24
Q

define allograft

A

grafts exchanged between nonidentical members of the same species

25
Q

define xenograft

A

graft exchanged between members of different species

26
Q

differentiate direct vs indirect allorecognition

A

direct: primary response against a graft. T cells recognize the donor MHC, directly

Indirect: T cells recognize donor MHC molecules that have been processed by recipient APCs

27
Q

differentiate between hyperacute, accelerated, acute, and chronic graft rejection

A

hyperacute: preformed antidonor antibodied and complement
accelerated: reactivation of sensitized T cells
Acute: primary activation of T cells
Chronic: both immunologic and nonimmunologic factors

28
Q

list the transplants (organs) that do not require ABO matching

A

corneal
heart valve
bone and tendon grafts

29
Q

define cross-matching and its role in determining transplant outcome

A

testing for preformed Abs in recipient’s blood against HLAs of transplant

30
Q

differentiate between acute and chronic GVHD

A

acute: epithelial cell death in skin, liver, and GI

Chronic: fibrosis and atrophy of affected organ

31
Q

mechanism of steroids (immunosuppressive)

A

anti-inflammatory

32
Q

mechanism of cyclosporin A (immunosuppressive)

A

inhibits IL-2 gene transcriptopn

is a peptide isolated from fungus that blocks calcium dependant activation of T-cells

33
Q

mechanism of anti-CD3 (OKT 3) monoclonal antibody (immunosuppressive)

A

T-cell activation (by blocking function of CD3 costimulator), opsonization and depletion

34
Q

mechanism of Tacrolimus (immunosuppressive)

A

inhibits IL-2 gene transcription

inhibits calcium dependent activation of t-cell

35
Q

mechanism of Anti-CD25 monoclonal antibodies

A

inhibits IL-2 function

36
Q

sirolimus

A

inhibits cytokine-mediated signal

37
Q

list the antibody mediated hypersensitivity types and the cell-mediated sensitivity types

A

antibody mediated: type I, II, III (against extracellular pathogens)

cell-mediated: type IV (defense against intracellular pathogens)

38
Q

describe some differentiating aspects of type I hypersensitivity

A

caused by release of mediators from mast cells

often triggered by IgE activation of the Th2 cells

39
Q

describe some differentiating aspects of type II hypersensitivity

A

abs specific for tissue (solid)

activate compliment by classical pathway

40
Q

describe some differentiating aspects of type III hypersensitivity

A

Ab-Ag complexes formed in circulation and cause vascular inflammation
soluble Ags

41
Q

describe some differentiating aspects of type IV hypersensitivity

A

T-cell mediated, delayed type hypersensitivity (DTH)
either due to autoimmunity or exagerated and persistent response to environmental factors
Th1 cells release IFN-gamma and TNF beta to activate macrophages

42
Q

systemic lupus erythematosus

A

type III hypersensitivity
clinical manifestation: rashes, arthritis, and glomerulonephritis
have many auto-abs and most common is anti-DNA abs which form complexes in circulation, stimulation of auto- ab secretion is result of activating B cells and isotype switching to IgG
diagnostic test: presence of anti-nuclear Abs

43
Q

Rheumatoid arthritis (RA)

A

type II but mainly type IV hypersensitivity
joint inflammation leading to joint and bone destruction
have auto-abs that react with their own Fc of IgG

44
Q

type I diabetes mellitus

A

type IV sensitivity

45
Q

Inflammatory bowel disease

A

type IV hypersensitivity

TNF plays big role

46
Q

what marks an allergy

A

presence of allergen specific IgE
mast cell and eosinophil recruitment
Th2 response and IL-4, IL-5, and il-13

47
Q

list the polymorphisms in genes known to be involved in atopy

A

beta chain of FcERIbeta (receptor of IgE)
IL-4
HLA-DR
CD14

48
Q

2 effects of hygiene hypothesis

A

shift from Th1 to Th2 type of immunity

decreased number/activity of Treg cells

Immunology (2 decks)

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