Immuno3 0519FA Flashcards

1
Q

passive immunity

A

acquired through PREFORMED Abs.
rapid onset.
short span of Ab (3 wks).

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2
Q

examples of passive immunity

A

IgA in breast milk.
antitoxin.
humanized monoclonal Ab.

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3
Q

active immunity

A

acquired through exposure to foreign Ags.
slow onset.
long-lasting protection (memory).

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4
Q

examples of active immunity

A

natural infx.
vaccines.
toxoid.

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5
Q

preformed Abs are given to pts after exposure to…?

A

Tetanus toxin.
Botulinum toxin.
HBV.
Rabies virus.

“To Be Healed Rapidly” with passive immunity

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6
Q

purpose of vaccines

A

induce ACTIVE immune response (humoral or cell-mediated) to specific pathogens

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7
Q

live attenuated vaccine

A

microorganism loses pathogenicity but retains capacity for transient growth within inoculated host

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8
Q

what kind of imm response is induced by live attenuated vaccine?

A

mainly cellular

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9
Q

pros of live attenuated vaccine

A

induces strong, often lifelong immunity

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10
Q

cons of live attenuated vaccine

A

may revert to VIRULENT form

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11
Q

examples of live attenuated vaccine

A

polio (Sabin).
MMR (measles, mumps, rubella).
varicella.
yellow fever.

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12
Q

inactivated or killed vaccine

A

pathogen inactivated by heat or chemicals.

maintain epitope structure of surface Ags is important for imm response.

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13
Q

what kind of imm response is induced by inactivated or killed vaccine?

A

humoral

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14
Q

pros of inactivated or killed vaccine

A

stable and safer than live vaccines

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15
Q

cons of inactivated or killed vaccine

A

weaker imm response.

BOOSTER SHOTS usually required.

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16
Q

examples of inactivated or killed vaccine

A
cholera.
influenza.
Hep A.
polio (Salk).
rabies.
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17
Q

autoAb: antinuclear Abs (ANA)

A

SLE, nonspecific

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18
Q

autoAb: anti-dsDNA, anti-Smith

A

SLE

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19
Q

autoAb: antihistone

A

drug-induced lupus

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20
Q

autoAb: anti-IgG (RHEUMATOID FACTOR)

A

RA

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21
Q

autoAb: anticentromere

A

scleroderma (CREST)

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22
Q

autoAb: anti-Scl-70 (anti-DNA topoisomerase I)

A

scleroderma (diffuse)

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23
Q

autoAb: antimitochondrial

A

primary biliary cirrhosis

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24
Q

autoAb: antigliadin, antiendomysial

A

Celiac disease

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25
Q

autoAb: anti-basement membrane

A

Goodpasture’s syndrome

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26
Q

autoAb: anti-desmoglein

A

pemphigus vulgaris

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27
Q

autoAb: antimicrosomal, antithyroglobulin

A

Hashimoto thyroiditis

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28
Q

autoAb: anti-Jo-1

A

polymyositis, dermatomyositis

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29
Q

autoAb: anti-SS-A (anti-Ro)

A

Sjogren’s syndrome

30
Q

autoAb: anti-SS-B (anti-La)

A

Sjogren’s syndrome

31
Q

autoAb: anti-U1 RNP (ribonucleoprotein)

A

mixed connective tissue disorder

32
Q

autoAb: anti-smooth muscle

A

autoimmune hepatitis

33
Q

autoAb: anti-glutamate decarboxylase

A

Type 1 diabetes mellitus

34
Q

autoAb: c-ANCA

A

Wegener’s granulomatosis

35
Q

autoAb: p-ANCA

A

other (non-Wegener’s) vasculitides

36
Q

macrophage cytokines

A
IL-1
IL-6
IL-8
IL-12
TNF-a
37
Q

IL-1

A
  1. endogenous pyrogen: fever, acute inflamm.
  2. activate endo to express adhesion molecs.
  3. induce chemokine secretion to recruit leukocytes.
38
Q

IL-6

A
  1. endogenous pyrogen: fever.

2. stimulate production of acute phase proteins.

39
Q

what cells release IL-6?

A

macrophages, Th2

40
Q

IL-8

A

major chemotactic factor for neutrophils.

and induce neutrophil phagocytic activity when they arrive

41
Q

IL-12

A
  1. induce differentiation of T cells into Th1 cell.

2. activate NK cells.

42
Q

what cells release IL-12?

A

macrophages, B cells

43
Q

TNF-a

A

“cachectin”

  1. septic shock
  2. activate endo.
  3. cause leuk recruitment, vasc leak.
44
Q

what cytokine is secreted by all T cells?

A

IL-3: supports growth and differentiation of BM stem cells (acts like GM-CSF)

45
Q

Th1 cytokines

A

IL-2

IFN-g

46
Q

IL-2

A

stimulates growth of all T cells

47
Q

IFN-g

A
  1. activate Th1 cells and macrophages (recruit leukocytes and activate phagocytosis).
  2. suppress Th2 cells.
  3. antiviral and antitumor.
48
Q

Th2 cytokines

A

IL-4
IL-5
IL-10

49
Q

IL-4

A
  1. induce differentiation into Th2 cells.
  2. promote growth of B cells.
  3. enhance class switch to IgE and IgG.
50
Q

IL-5

A
  1. promote differentiation of B cells.
  2. enhance class switch to IgA.
  3. eosinophil growth and diff.
51
Q

IL-10

A

anti-inflamm:

  1. inhibits action of activated T cells, Th1.
  2. activate Th2.
52
Q

what cells secrete IL-10?

A

Th2 cells, regulatory T cells

53
Q

what other cytokine acts like IL-10?

A

TGF-b: also inhibits inflamm

54
Q

interferon mechanism

A

induce prod of RIBONUCLEASE that inhibits viral protein synth by degrading viral (not host) mRNA – places uninfected cells in an ANTIVIRAL state.

*also activate NK cells to kill virus-infected cells

55
Q

what do IFN alpha and beta do?

A

inhibit viral protein synth

56
Q

what does IFN gamma do?

A

increase MHC I and II expression

and Ag presentation in all cells

57
Q

cell surface proteins of T cells

A

TCR: binds Ag-MHC complex.

CD3: assoc w/ TCR for signal transduction.

CD28: binds B7 of APC.

also…
CD4: helper T cells.
CD8: cytotoxic T cells.

58
Q

cell surface proteins of B cells

A

Ig: binds Ag.

CD19, 20, 21, 40.

MHC II and B7: APC fx.

59
Q

which B cell surface proteins is a receptor for EBV?

A

CD21

“you can drink Beer at the Bar when you’re 21”

60
Q

cell surface proteins of macrophages

A

CD14, 40.

MHC II and B7.

Fc and C3b receptors: enhance phagocytosis.

61
Q

cell surface proteins of NK cells

A

CD16: bind Fc of IgG.

CD56: unique to NK cells*

62
Q

what are the ONLY mature cells in the body to NOT have MHC I?

A

RBCs

63
Q

anergy

A

without costimulatory molecule, self-reactive T cells become nonreactive

*in B cells, anergy also happens but tolerance is less complete

64
Q

superantigens

A

cross-link beta-region of TCR to MHC II on APCs = uncoordinated release of IFN-g from Th1 and subsequent release of IL-1, IL-6, TNF-a from macrophages

65
Q

what microorganisms produce superantigens?

A

S.pyogenes

S.aureus

66
Q

endotoxins (LPS)

A

directly stimulate macrophages by binding endotoxin receptor, CD14 (Th cells not involved)

67
Q

what microorganisms produce endotoxins (LPS)?

A

gram negatives

68
Q

Ag variation in bacteria: Salmonella

A

2 flagellar variants

69
Q

Ag variation in bacteria: Borrelia

A

relapsing fever

70
Q

Ag variation in bacteria: Neisseria gonorrhoeae

A

pilus protein

71
Q

Ag variation in virus: influenza

A

major: antigenic shift.
minor: antigenic drift.

72
Q

Ag variation in parasite: trypanosome

A

programmed rearrangement