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Basic Immunology- Module 1 > Complement > Flashcards

Complement Flashcards

1
Q

What are the main effector functions in complements role in killing of microbes?

A

opsonisation; leukocyte activation and cell lysis

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2
Q

What complement factor is involved in the activation of leukocytes?

A

C5a

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3
Q

What are the functions of complement?

A

killing of microbes; briding innate and adaptive immunity; immune complex processing; removal of apoptotic cells

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4
Q

What are the functions of C5a?

A

potent anaphylatoxin; chemotaxis; endothelial activation; prothormbotic

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5
Q

What are the functions of C5b-9?

A

cell lysis; platelet activation; endothelial activation; prothrombotic

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6
Q

How is the classical pathway of complement activated?

A

by binding of C1q to Fc portions of IgG and IgM or recognises microbial surface directly

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7
Q

How is the lectin pathway of complement activated?

A

mannose binding lectin and ficolins interacting with bacterial carbohydrate residues

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8
Q

How is the alternative pathway of complement activated?

A

spontaneously

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9
Q

What is a zymogen?

A

inactive pro-enzyme which become activated after proteolytic cleavage

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10
Q

What associates with MBL and ficolins to trigger cleavage of complement?

A

MBL-associated serine proteases (MASPs)

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11
Q

What is C1 comprised of?

A

recognition protein C1q assocated with proteases C1s and C1s

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12
Q

What do all 3 complement pathways generate?

A

C3 convertase

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13
Q

What is C3 convertase?

A

a multisubunit protein with protease activity that cleaves complement component 3 (different types depending by pathway)

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14
Q

what is the main effector molecules of the complemetn system?

A

C3b

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15
Q

Where does C3 convertase cleave C3?

A

when it is bound covalently to the pathogen surface releasing C3a while leaving lots of C3b bound to the surface

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16
Q

What is the function of C3a?

A

binds to specific receptors and helps induce inflammation

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17
Q

What is C3b degraded into?

A

C3f and C3dg

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18
Q

How does covalent bond formation between C3b and the pathogen surface take palce?

A

due to highly reactive thioester bond hidden inside the folded C3 protein

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19
Q

What are the components of C3 convertase in the lectin and classical pathways?

A

C4b2a

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20
Q

What are the compoents of C3 convertase in the alternative pathway?

A

C3bBb

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21
Q

What is the difference in glycans between yeast and vetebrates?

A

yeast glycans terminate in mannose resudes rather than sialic acid residues

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22
Q

Where is MBL synthesised?

A

liver

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23
Q

What is a collectin?

A

protein that has an amino-terminal collagen-like domain and a carboxy-terminal C-type lectin domain

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24
Q

What is the difference in structure between ficolins and MBL?

A

ficolins have a fibrinogen-like domain rather than lectin domain

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25
Q

How many types of ficolin do humans have?

A

L-ficolin (2); M-ficolin (1) and H-ficolin (3)

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26
Q

Where are the ficolins produced?

A

L and M ficolins are produced by the liver; M-ficolin is procued by lung and blood cells

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27
Q

What happens when MBL bound to MASP 1,2 and 3 binds to a pathogen surface?

A

MASP-1 is conformationally changed and activates MASP-2 which can cleave C4 and C2

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28
Q

What happens to C4 once activated by MASP-2?

A

similarly to C3, C4b has a reactive thioester which binds to pathogen surface

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29
Q

What happens to C2 once activated by MASP-2?

A

C2a remains bound to C4b

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30
Q

What is the function of C4bC2a?

A

cleaves many molecules of C3 into C3b and C3a

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31
Q

Give examples of other collectins?

A

surfactant proteins A and D

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32
Q

What is the function of surfactnat proteins A and D?

A

coat surfaces of pathogens to opsonise

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33
Q

why do SP-A and SP-D not activate complement?

A

don’t associated iwth MASPs

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34
Q

What happens when the globular heads of C1q bind to ligand?

A

conformational change in C1r:C1s complex- activating C1r which then cleaves C1s

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35
Q

What does activated C1s do?

A

cleaves C4 into C4a and C4b which binds to pathogen surface, a molecule of C2 binds to C4b which is then cleaves by C1s to C2a

36
Q

How does C1q bind to pathogen?

A

directly; via CRP and binds to the Fc regions of antibodies bound to antigen

37
Q

What prevents C4b from diffusing from its site of activation to becoming attached to htealth host cells?

A

the thioester bond is rapidly hydrolysed and irreversibly inactviated

38
Q

What are the 2 ways that the alternative pathway can be activated?

A

by the action of the lectin or classical pathways; spontaneous hydrolysis

39
Q

How can the alternative pathway be activated by the lectin/classical patwhays?

A

C3b bound to the pathogen surface binds factor B whih is then cleaved by plasma protease factor D into Ba and Bb forming C3bBb`

40
Q

What is fluid-phase C3 convertase?

A

C3(H2O)Bb

41
Q

What stabilises the alternative pathway C3 convertases?

A

properdin (factor P)

42
Q

Where is properdin synthesised?

A

neutrohpils

43
Q

What is significant about hte alternative pathway?

A

amplification loop to increase C3b production rapidly

44
Q

What do ficolins bind to?

A

acetylated sugar residues

45
Q

What does a H-ficolin deficiency lead to?

A

necrotising entercolitis

46
Q

What does mutations in MASP3 or CL-K1 lead to?

A

3MC syndrome- developmental abnormalities and mental retardation

47
Q

What is the active enzyme of the C3/C5 convertases?

A

C2a

48
Q

What is DAF/CD55?

A

decay-accelerating factor - complement-regulatory protein

49
Q

How does DAF work?

A

competes with factor B for binding to C3b and can displace Bb from a convertase

50
Q

What is the function of factor I in complement?

A

cleaves C3b to iC3b an inactive derivative

51
Q

What is required for factor I to work?

A

cofactors- membrane cofactor of proteolysis (MCP/CD46)

52
Q

Name a protein that has similar actions of DAF and MCP (inhibits convertase formation and inc. breakdown of C3b)?

A

CR1/CD35- cell-surface complement receptor type 1

53
Q

What are teh function of factor H?

A

competes with factor B; acts as cofactor for factor I

54
Q

What is significant about factor D?

A

only activating protease of hte complement system to circulate as an active enzyme rather than zymogen

55
Q

How is C5 convertase generated in the classical and lectin pathways?

A

binding of C3b to C4b2a

56
Q

How is C5 convertase generated in the alternative pathwat?

A

binding of C3b to C3bBb to form C3b2Bb

57
Q

How does C5 convertase cleave C5?

A

C5 has to bind to C3b on C5 convertase and can then be cleaved by C2a or Bb

58
Q

What complement receptor does C3b bind to?

A

CR1

59
Q

What is required to activate phagocytosis when C3b binds to CR1?

A

C5a

60
Q

What else does C5a bind to aside from CR1?

A

C5a receptor- a GPCR

61
Q

What receptors bind forms of C3b which have been cleaved by factor I but which remain attached to pathogen surface?

A

CR2; CR3 and CRIg

62
Q

What does CR2 recognise?

A

C3dg

63
Q

How is C3dg produced?

A

C3b is cleaved releasing C3f to form iC3b; which is then cleaved to release C3c leaving C3dg

64
Q

What cells have CR2?

A

B cells - amplifies antibody response

65
Q

What is the function of binding of iC3b to CR3?

A

sitmulates phagocytosis

66
Q

Give eamples of circulating regulators of complement?

A

C1 inhibitor; C4-binding protein and factor H

67
Q

What is the role of CD59 as a regulator?

A

prevents assembly of MAC

68
Q

When does factor H preferentially bind factor C3b?

A

when it is boudn to vertebrate cells

69
Q

What is complementopathy?

A

pathology arising from abnormal complement activation

70
Q

What diseases can result from overactivation o the complement system?

A

paroxysmal nocturnal haematuria; atypical HUS; C3 glomerulopathy; macular degeneration; IgA nephroptahy

71
Q

How does a pore in thel ipid bilayer membrane caause pathogen death?

A

destroying the proton gradient

72
Q

which part of the MAC binds to the lipid bilayer?

A

C7 amphiphilic copmlex

73
Q

What is the function of C9n?

A

polymerizes C5b678 to form a membraen-spanning channel, lysing the cell

74
Q

What part of the MAC inserts into the lipid bilyaer?

A

C8a-y

75
Q

what does a deficiency in C5-C9 result in?

A

vulnerability to Neisseria species

76
Q

What is C1 inhibitor?

A

a plasma serine protease inhibitor or serpin

77
Q

What is the function of C1 inhibitor?

A

binds to the active enzymes C1r:C1s and causes them to dissociate from C1q and also limits the spontaneous activation of C1 in plasma

78
Q

What complement levels are low in C1 inhibitor defieicny ?

A

C4 (being used up a lot)

79
Q

What does C1INH inhibit in the coagulation system?

A

factor XI and thrombin

80
Q

What does C1INH inhibit in the bradykinin system?

A

kallikrein ( inhibits bradykinin)

81
Q

What proteins are affected in PNH?

A

decay-acclerating factor (inactivates membrane C3 convertase); CD59 (prevents MAC assembly)

82
Q

What treatment can be give to patietns with PNH?

A

eculizumab- monoclonal ab against C5

83
Q

What are the risks and benefits of eculizumba?

A

reduces blood transfusions but increases risk of meningitis (C5 important against neisseria)

84
Q

What happens in atypical haemolytic uraemic sydnrome?

A

C5 mediated damage to the renal endothelium leading to glomerular thrombosis

85
Q

What drug is highly effective in atypical HUS?

A

eculizumab

Basic Immunology- Module 1 (31 decks)

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