SFM Immuno Exam 1 Flashcards

1
Q

TNF, IL-1, chemokines

A

Function: pro-inflammation

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2
Q

INF-a, IFN-B

A

resistance to viral infection

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3
Q

IFNy

A

macrophage activation

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4
Q

IL-12

A

IFNy production (by NK cells and T cells)

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5
Q

IL-15

A

Proliferation of NK cells

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6
Q

IL-10, TGF-B, IL-4

A

control of inflammation (anti-inflammatory)

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7
Q

IL-1, TNFa, IL-6

A

secreted by Tissue macrophage, enter bloodstream and produce systemic effects (acute phase response)

  • fever (IL-1, TNFa, IL-6)
  • induction of acute phase proteins (IL-6, IL-1, TNFa)
  • althralgia/myalgia (TNF-a)
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8
Q

IL-2

A

Growth factor for T cells, makes resistant to apoptosis

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9
Q

IL-8

A

chemokine for neutrophils, stimulate conformational changes in ICAM-1 and VCAM1

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10
Q

MCP-1

A

chemokine for monocytes, stimulates conformational changes in ICAM-1 and VCAM1

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11
Q

PAMPS

A

pathogen associated molecular proteins

recognized by PRR (pattern recognition receptors)

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12
Q

TLR2/TLR6

A

recognizes gram positive bacteria

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13
Q

TLR4

A

recognizes gram negative bacteria

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14
Q

CR1

A

copmlement receptor type 1: on surface of macrophage or neutrophil, binds C3b after it has bound to pathogen survace

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15
Q

Th1 (T helper 1)

A

cells control against intracellular pathogens

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16
Q

Th2 (T helper 2)

A

control responses against extracellular pathogens,

also promote production of antibodies by B cells

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17
Q

Dendritic cells direct diff of T. cells

A

into T helper 1 cells or T helper 2 cells

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18
Q

TLR3

A

double stranded (viral) RNA

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19
Q

TLR5

A

flagella

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20
Q

TLR9

A

unmethylated CpG DNA

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21
Q

C1 (CP)

A

initiates classical pathway

22
Q

C1q (CP)

A

binds to Fc portion of Ab that has antigen bound to apoptotic cells and cell surfaces

23
Q

C1r (CP)

A

serine protease, cleaves C1s to make active

24
Q

C1s (CP)

A

serine protease, cleaves C2 and C4

25
Q

C4

A

covalently binds to microbe to activate complement. C4b binds C2 for cleavage by Cls

26
Q

C2

A

C2 serine protease and functions as active enzyme of C3 and C5 convertases to cleave C3 and C5

27
Q

MBL (LP)

A

agglutinin, opsonin, complement fixing

28
Q

MASP1 (LP)

A

forms complex with MASP2 and collectins or ficolins, activates MASP2-3

29
Q

MASP2 (LP)

A

forms complex with lectins esp. ficolin-2.

- cleaves C4 and C2

30
Q

CP and LP C3 convertase

A

C4bC2a

  • after cleaving C3 (to C3b and C3a - opsonin)
  • forms C4bC2aC3b (C5 convertase)
31
Q

CP and LP C5 convertase

A

C4bC2aC3b

- cleaves C5 to C5a (opsonin) and C5b (activates MAC)

32
Q

AP C3 convertase

A

C3bBb

33
Q

AP C5 convertase

A

C3bBbC3b

34
Q

Complement regulatory proteins

A

prevent complement system from activating on human cells (for lysis)

35
Q

C1 inhibitor (C1 INH)

A

complement regulatory protein

inactivates C1r, C1s, MASP1, MASP2

36
Q

MCP

A

complement regulatory protein

cofactor for factor 1 mediated cleavage C3b and C4b

37
Q

DAF

A

complement regulatory protein

destabilizes C3/C5 convertases of CP and AP

38
Q

CR-1

A

complement regulatory protein

cofactor for facor 1 mediated cleavage of C3b and C4b

39
Q

C4 Binding protein (C4BP)

A

complement regulatory protein

binds to C4b, decay accelerating and cofactor activity

40
Q

Factor H

A

complement regulatory protein

Binds to C3b - has decay accelerating activity of AP c3 and C5 convertases and cofactor activity

41
Q

CD59

A

complement regulatory protein

blocks C9 association 2 C5b-8 to prevent C5b-9 form on host cells

42
Q

S protein

A

vitronectin binds to C5b-7, inhibis C9 polymerization

43
Q

Disease from C1, C2, C4 Deficiency

A

immune complex disease (all pathways)

44
Q

Disease from C3 Deficiency

A

susceptibility to capsulated bacteria

45
Q

Disease from C5-C9 Deficiency

A

susceptibility to Neisseria (no MAC)

46
Q

Disease from Factor 1 Deficiency

A

susceptibility to capsulated bacteria

47
Q

Disease from Factor D, properdin (Factor P) Deficiency

A

susc. to capsulated bacteria and neisseria, no immune complex disease

48
Q

Disease from DAF, CD59 Deficiency

A

Autoimmune-like conditions including PNH

49
Q

Disease from C1-INH Deficiency

A

hereditary angioedema - due to buildup of bradykinin

C1-INH inactivates plasma kallikrein, cleaves plasma kininogen to produce bradykinin

50
Q

systemic lupus - Glomerulonephritis

A

local activation of complement and production of C3a and C5a, recruits inflammatory cells and further aggravates
- MAC mediated injury to glomerulus due to overactive complement