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Immunology > Complement System > Flashcards

Complement System Flashcards

1
Q

Complement system is defense against

A

mainly bacteria

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2
Q

proteins for CS are synthesized in

A

the liver

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3
Q

many CS proteins are present as

A

inactive form in blood and other fluids and require activation for effect

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4
Q

activation pathways

A

classical(CP), Alternative(AP) and Terminal(TP)

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5
Q

a deficiency in the terminal pathway components leads to

A

susceptibility to Neisseria Sp infections

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6
Q

Membrane attack complex (MAC)=

A

in terminal/common C5b, C6, C7, C8, C9

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7
Q

activation of classical pathway leads to

A

convergence with terminal pathway

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8
Q

Activation of classical pathway starts with

A

IgG(2 Fc’s needed) or IgM(only 1 needed) complex binds to C1

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9
Q

Pentameric IgM=

A

5Fc-mu’s available to bind

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10
Q

C1 cleaves

A

C4 to C4a and C4b and C2 to C2a and C2b

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11
Q

C1 Cleavage forms

A

C4b2a= C3 convertase(CP)

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12
Q

C3 convertase cleaves

A

C3 to C3a and C3b and forms C4b2a3b (C5 convertase)

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13
Q

C5 convertase cleaves

A

C5a and C5b

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14
Q

C5b binding to

A

the microbe surface initiations formation of MAC of the Terminal pathway

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15
Q

Alternative pathway is activated by

A

spontaneously generated C3b deposits on activating surface

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16
Q

Factor B binds to

A

C3b

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17
Q

Factor B is cleaved by

A

Factor D and forms teh C3bBb

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18
Q

C3bBbis also called

A

C3 convertase

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19
Q

Poperdin extends

A

the half life of C3bBb by 6-10 fold

20
Q

C3bBb cleaves

A

C3 to C3a and C3b and forms C3bBb3b (C5 convertase)

21
Q

C3bBb3b cleaves

A

C5 to C5a and C5b

22
Q

classical proteins

A

C1,2,3,4,5

23
Q

Terminal proteins

A

C5b, 6,7,8,9

24
Q

Alternative proteins

A

C3b,3,5 Factor B, D Properdin

25
Q

role of C3b

A

opsonin mediated phagocytosis and elimination of immune complexes

26
Q

role of C3a, 4a, 5a

A

degranulation of mast cells and basophils

27
Q

Role of C5a

A

chemotaxis of neutrophils

28
Q

role of MAC

A

Osmotic lysis of bacteria

29
Q

role of regulatory complement proteins

A

protect autologous cells from complement mediated damage

30
Q

C1 INH, C1 esterase inhibitor binds

A

C1 to prevent spontaneous activation

31
Q

C4bp(binding protein binds

A

the fluid phase of C4b preventing attachment to cells and formation of C3 convertase

32
Q

Factor H binds

A

to C3b in fluid phase preventing the binding to the microbe

33
Q

Factor H competitively binds

A

C3b which leads to dissociation of C3bBb if it has formed.

34
Q

Decay accelerating Factor (DAF)

A

binds to membrane bound C3b or C4b blocking formation of C3 convertase or dissociating C3 convertases that formed.

35
Q

Anaphylatoxin inhibitor binds

A

C3a, C4a and C5a and inhibits binding to Cr3a/4a. C45a

36
Q

Factor I cleaves

A

C4b and C3b to inactive forms in presence of cofactors

37
Q

S- protein, CD59, and Homolgous restriction factor (HRF

A

inihibit formation of MAC on autologous cells.

38
Q

CR1

A

receptor on phagocytes and RBC that binds to C3b or C4b and is part of the opsonin/immune complex elimination

39
Q

CR2

A

receptor on B cells that binds C3bi- is a mode of epstein barr virus infection

40
Q

C3a/4a binds

A

C3a and C4a and is found on mast cells and basophils, it leads to degranulation and histamine release (CR5a binds C5a on mast cells and basophils for the same effect

41
Q

CR5a on neutrophils binds

A

C5a which is used as a chemotaxis for neutrophils

42
Q

Ch50 complement test

A

measures overall complement activity and whether or not it is low for c3 and c4

43
Q

Tissue damage activates

A

the intrinsic coagulation system and activates factor XII

44
Q

factor XII(a) activates

A

zymogen prekallikrein to kallikrein

45
Q

role of kallikrein

A
  • -cleave kininogen to kininogena and brady kinin

- -cleaves C5 to C5a and C5b because C5a is chemotactic for neutrophils

46
Q

bradykinin increases

A

vascular permeability which is critical in inflammation

47
Q

Killikrein is inactivated by

Immunology (14 decks)

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