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quiz 2 Flashcards

1
Q

type I hypersensitivity mechanism

A

sensitization: allergen elicits strong Th2 response, causing B cell isotype switch→IgE via IL-4 and IL-14, coats mast cells.
2nd exposure: sensitized mast cell→secretes arachidonic acid mediators (prostaglandins for vascular dilation, smooth muscle contraction), degranulates (histamine→local inflammation), and cytokines like TNF for late phase reaction, recruit PMNs and eosinophils (activated by IL-5 from mast and Th2; releases proteases for tissue damage)

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2
Q

symptoms and treatment for type I hypersensitivity

A

hay fever, food allergies, bronchial asthma and anaphylaxis (systemic edema with ↓BP). treat with antihistamines, steroids, or SCIT (hyposensitization via subcutaneous admin of antigen in increasing doses, stimulating Tregs and IgG, divert response away from IgE)

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3
Q

type II hypersensitivity (cytotoxic)

A

anti-tissue Abs bind to targets in cells/ECM→tissue injury via recruitment of cytolytic effectors, via IgM, IgG, complement-mediated lysis (C3a, C3b, C5a) and phagocytosis and Ab-mediated cellular toxivity

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4
Q

transfusion reactions

A

alloantibodies against A or B antigen occur if RBC/endothelium doesnt express. example of cytotoxic/type II hypersensitivity

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5
Q

hemolytic disease of the newborn

A

Rh- mother makes anti-D antibodies which can hurt next RhD fetus because IgG can cross placenta. Example of type II/cytotoxic hypersensitivity. treat w/ rhesus prophylaxis (anti-RhD antibodies). less common if also have ABO mismatch

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6
Q

autoimmune blood dyscrasias

A

type II cytotoxic hypersensitivity. antibodies against own RBC/platelet/lymphocyte/PMN, get eliminated via cytotoxic II rxn→anemia, etc. Or, Abs get made against hapten drugs bound to host cell, and whole complex gets destroyed. test for w/ direct coombs test

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7
Q

hyperacute graft rejection

A

type II/cytotoxic. anti-graft endothelium antibodies pre-existing in host attack, activate complement/clotting, cause endothelial injury/thrombus.

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8
Q

TRALI

A

type II/cytotoxic. Abs in donated plasma against neutrophils or HLA bind recipient, can be deadly

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9
Q

Goodpastures syndrome

A

type II/cytotoxic. Abs against lung/kidney basement membrane.

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10
Q

type III/immune complex disease mechanism

A

immune complexes of antigen, Ab and complement end up in vasculature because of IgM and IgG mediated rxn to excess antigen. Complex activates complement →C3a and C5a→bind to mast and endothelium, cause vascular permeability, PMN recruitment→PMNs secrete B4 and IL8→tissue damage via release of leukotrienes C4, D4, and TNF from PMN, macrophages and masts.

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11
Q

clearance of immune complexes

A

via phagocytosis (macrophage/monocyte) via C3b receptor on RBC, complement, PMN and phagocytes.

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12
Q

serum sickness

A

type III/immune complex. systemic protein antigen (usually another species’ abs) causes systemic immune complex circulation. deposits removed by macrophage/neutrophil via IgG Fc receptors from local inflammatory response and complement activation and mediator release. Soluble ICs get deposited on BM and are cleared by neutrophils eventually (via IL8 and B4 and C5a taxis)

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13
Q

arthus reaction

A

type III/immune complex. localized immune complex reaction due to subcutaneous admin of excess protein antigen to previously immunized animal→local erythema and edema.

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14
Q

immune complex detection

A

C1q binding; isolate IC in assay, immobilize in solid phase and detect with anti-human Ab. CH50: total hemolytic component of blood→indirect measurement of IC. immunohistology.

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15
Q

Type IV/delayed type hypersensitivity (DTH)

A

Th1 cells (not antibodies) mediate reaction to a prior-sensitized intracellular antigen–>activate macrophages via IFN-gamma to ingest/kill infected cells. used to show prior exposure to a mycobacterial antigen. starts 24-28h after challenge.

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16
Q

tuberculin-type hypersensitivity

A

cutaneous delayed DTH, i.e. mantoux reaction. 12-24 hours following inoculation, site is indurated and erythemous. peak 1-2 days, lymphocyte and macrophage presence. indicates active or latent infection, prior infection or vaccination.

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17
Q

contact hypersensitivity

A

DTH: small molecules (plants, metals in jewelry, poison ivy/oak) taken up and interact w/ skin proteins to become complete antigen→elicits T cell activation (CD4). Re-exposure→contact dermatitis (erythema, itching, besicles, eczema, etc.) because of attack by CD8 cells. symptoms 4-96h, peak @1-14 days.

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18
Q

granulomatous hypersensitivity

A

DTH: persistent antigen from difficult-to-remove organism (leprosy, TB)–remains in granuloma (collection of activated lymphocytes and macrophages around microbe w/ fibrosis and tissue necrosis). causes sustained immune rxn with local tissue damage.

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19
Q

cross-reactive epitopes

A

foreign antigen autoimmunity; common epitope to antigen and host, i.e. strep and heart tissue

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20
Q

FAs in circulation

A

FA autoimmunity. immune complexes w/ FA cause local tissue damage when cleared.

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21
Q

FA as adjuvant

A

FA autoimmunity; microbes like epstein-barr and coxsackie stimulate greater expression of TLRs, which can make a weak self-reaction stronger.

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22
Q

sequestered antigen theory

A

autoantigen mechanism: self epitopes not present during immunocompetence induce autoimmunity.

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23
Q

immunologic deficiency theory

A

autoantigen mechanism: deficient immune response causes persistent infection and inflammation leading to modified autoantigens or uncovering of sequestered antigens

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24
Q

mechanisms of autoimmunity

A 
autoAbs:
mediate cell destruction
interfere w/ normal receptor function
form precipitating immune complexes that damage tissue
cause endocrine dysfunction
25
Q

autograft

A

donor=recipient, no rejection

26
Q

syngeneic graft

A

aka isograft, syngraft: 2 genetically identical individuals

27
Q

allograft

A

2 genetically different individuals of same species; rejection if no immunosuppression

28
Q

xenograft

A

2 individuals of 2 different species, rejection because of antibody disparity

29
Q

bone marrow graft

A

immune cell graft; risk rejection and immune response from donor marrow against host tissue (graft vs host disease)

30
Q

transplant rejection

A

H antigens are MHC from allograft; rejection if donor has H antigens absent in host. strong immune response because many lymphocytes are alloreactive (preprogrammed for MHC, 2-10% of T cells)

31
Q

immune response against transplant

A

usually cell mediated, esp. CD4. MHC II mismatch worse than MHC I. Memory-forming. abundance of lymph channels∝strength of rejection. can be direct recognition (allogeneic MHC on graft APC recognized by host T) or indirect recognition (allogeneic MHC digested and presented by host APC)

32
Q

hyperacute graft rejection

A

circulating, pre-existing host antibody against donor endothelial cell antigens; ischemic necrosis at graft, inflammation. minutes-hours

33
Q

acute graft rejection

A

days-weeks- primary cause of early graft RJ. mediated by CD8 cells and Igs against parenchymal and endothelial cells of graft.

34
Q

chronic graft rejection

A

months-yearsl progressive loss of graft function; probably an extended DTH mediated by CD4 cells against graft alloantigens –>vessel occlusion.

35
Q

BCG and cholera vaccine

A

live attenuated or killed bacteria

Ab response + CD4

36
Q

Polio vaccine

A

live attenuated virus (OPV, sabin)
used to be killed baccine (IPV, salk)

cell mediated immunity + ab response

37
Q

tetanus and diphtheria toxoid vaccine

A

subunit (antigen) vaccines

antibody response

38
Q

haemophilus influenzae vaccine

A

conjugate vaccine

CD4-dependent Ab response to polysaccharide antigens

39
Q

hepatitis vaccine

A

synthetic vaccine

antibody response

40
Q

live attenuated vaccines

A

i.e. diphtheria, MMR, pertussis, polio

organism grown in non-optimal conditions to make less virulent but still immunogenic. can be infectious in IS ppl.

41
Q

killed vaccines

A

i.e. rabies, cholera

no t-cell response, less efficacious, no IgA, shorter duration of protection.

42
Q

conjugate vaccines

A

typical for bacteria

hapten-carrier construct: covalently attached polysaccharide antigen (B-cell epitope) + carrier protein (T-cell epitope)

43
Q

toxoid-based vaccines

A

chemical/heat treated toxins–>inactive but immunogenic.

44
Q

subunit vaccines

A

no disease potential; need adjuvants to enhance immune response.

45
Q

Bruton’s disease

A

primary immunodeficiency
form of XLA: congenital agammaglobulinemia where defective RTK gene (btk) prevents pre-B–>B cell maturation. No opsonization, less phagocytosis.

46
Q

CVID

A 
primary immunodeficiency (b-cell related)
no CD4 helping B cells. Low IgG and IgA (most commonly).
47
Q

Hyper IgM syndrome

A

primary b immunodeficiency

No isotype switching b/c defect in CD40/CD40L

48
Q

DiGeorge syndrome

A

primary T ID

absent/small thymus

49
Q

bare lymphocyte syndrome

A

primary T ID

defective MHC II–>no CD4–>phenotype of SCID.

50
Q

TAP1/2 defects

A

primary T ID

lack of MHC I, CD8 deficiency

51
Q

WAS (Wiskott-Aldrich syndrome)

A

primary T ID

mutation affecting cytoskeletal signalling

52
Q

Ataxia-telangiectasia

A

primary T ID

impaired lymphocyte development (TCR and BCR) due to mutation in ATM protein (DNA repair checkpoint)

53
Q

SCID

A

primary ID
B and T cell development impaired by cytokine gamma chain defect, affecting IL-2, 4,7,9,15, T and NK cells. Can have lymphocyte toxicity due to purine metabolite buildup, or defects in DNA recombination enzymes–>nonfunctional Ab or TCR.

54
Q

cyclic neutropenia

A 
primary ID (phagocyte)
too few PMNs due to stem cell differentiation defect
55
Q

LAD

A 
primary ID (phagocyte)
lack of adhesion to endothelium
56
Q

complement component deficiencies

A

primary complement-related ID
C3: recurrent infections of encapsulated bacteria, like neisseria/pyogenic bacteria.
C1,2,4: immune complex disease
MAC (C5-9): neisseria infxns.

57
Q

hereditary angioedema

A

primary complement-related ID

C1q inhibitor deficiency results in continuous complement activation and consumption.

58
Q

secondary immunodeficiency

A

AIDS, immune senescence.

immuno (2 decks)

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