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Immunology & Serology (Lecture) > The Complement System > Flashcards

The Complement System Flashcards

1
Q

System of plasma proteins which completes the process initiated by the interaction of antigen and antibody combination-lysis

A

complement system

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2
Q

Series of more than ________ that interact to enhance host defense reactions

A

more than 25 serum proteins

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3
Q

Most are _________ that are converted to active enzymes in a precise order

A

inactive enzyme precursors

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4
Q

It constitutes ________, heat labile that are present in normal human serum and all tissue fluids except urine and CSF

A

5% of normal serum protein

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5
Q

The key mediator in all pathways

A

C3

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6
Q

Sequential activation of complement components occurs via one of the three pathways

A

Classical Pathway
Alternative Pathway
Lectin Pathway

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7
Q

Initiated by formation of antigen-antibody complex

A

Classical pathway

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8
Q

Initiated by foreign cell surface; antibody independent ; part of innate immunity

A

Alternative pathway

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9
Q

Initiated by host proteins binding microbial surface

A

Lectin pathway

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10
Q

CASCADE ACTIVATION
Complement proteins are often designated by an
uppercase letter C and are inactive until they are split into products

A

C1

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11
Q

CASCADE ACTIVATION
When the products are split they become active. The
active products are usually designated with a lower
case a or b

A

C1a and C1b

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12
Q

All classes of immunoglobulin do not fix complement
only ______, ______, ______, and ______ fix in the respective order

A

IgM, IgG3, IgG1 and IgG2

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13
Q

These Ig do not fix complement

A

IgG4, IgA, IgD and IgE

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14
Q

Complement does not bind to ______ and ______

A

antigen and antibody

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15
Q

Activated by antibodies bound to antigen

A

classical pathway

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16
Q

Activated on microbial cell surfaces in the absence of antibody

A

alternative pathway

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17
Q

Activated by plasma lectin that binds to mannose residues on microbes

A

lectin pathway

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18
Q

4 important functions of complement system

A

lysis
opsonization
activation of inflammatory response
clearance of immune complexes

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19
Q

Overview of the complement pathways indicating
components required for _______, _______, _______. ______, and _______

A

recognition, enzymatically active components and complexes, major opsonic, inflammatory, and membranolytic products

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20
Q

4 components of alternative pathway

A

C3, factor B, factor D, properdin

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21
Q

Triggering substances may be pathogens or nonpathogens:
○ Bacterial cell wall components
○ Fungi
○ Viruses
○ Parasites
○ Immune complexes
○ RBCs
○ Polymers

A

alternative pathway

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22
Q

activation of alternative pathway

A

proteolysis of C3

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23
Q

Binding site for factor B covalently tethered to surface of microbial or host cell

A

C3b

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24
Q

Bound factor B cleaved by ________

A

factor D (serine protease)

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25
Q

C3 convertase

A

C3bBb

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26
Q

Properdin bind to and stabilize _________

A

C3bBb complex

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27
Q

C5 convertase

A

C3bBb3b

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28
Q

A protein that binds to CHO

A

lectin

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29
Q

It binds to mannose on many bacterial cells

A

mannose-binding lectin pathway (MBL)

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30
Q

It produced by liver in acute phase inflammatory reactions

A

MBL

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31
Q

Once MBL binds to target cell, 2 serine proteases _______ and _______ bind

A

MASP-1, MASP-2

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32
Q

acts like C1

A

MBL pathway

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33
Q

an acute phase protein, binds to mannose residues

A

MBL

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34
Q

When MBL complex binds to a pathogen surface, MASP-2 is activated to cleave _____ and _____

A

C4 and C2

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35
Q

Importance in innate host defense mechanism in early childhood

A

MBL pathway

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36
Q

activation of MBL pathway

A

D-mannose, GIcNAc (microbial polysaccharides)

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37
Q

Binding to circulating lectins, [e.g., Mannose-binding
lectin (MBL), or to _________ recognizing lectins (ficolins) collectin family and structurally resemble C1q

A

N-acetylglucosamine

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38
Q

MASP-1 cleaves to _____

A

C3

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39
Q

MASP-2 cleaves to _____ and _____

A

C4 and C2

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40
Q

C3 convertase

A

MASP-1

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41
Q

C5 convertase

A

C4b2b3b

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42
Q

regulation of the complement cascade
short half life of:

A

C3b, C3bBb, C5b

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43
Q

It inhibits the C1s activity

A

C1 inhibitor

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44
Q

Glycophosphatidylinositol-linked membrane protein

A

DAF

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45
Q

On endothelial cells and erythrocytes

46
Q

If deficiency, causes Paroxysmal Nocturnal Hemoglobinuria (PNH)

47
Q

Unusual feature, acquired mutation in defective gene, in hematopoietic stem cells

48
Q

Plasma serine protease degrade cell-associated C3b

49
Q

Active only in presence of regulatory proteins

50
Q

MCP, factor H, C4BP, and CR1 serve as cofactors

51
Q

Cause dissociation of C3b (and C4b)-containing complexes

52
Q

Generates iC3b, C3d, and C3dg, recognized by receptors on phagocytes and B lymphocytes

53
Q

regulators of the C3 and C5 convertase

A

DAF
factor 1

54
Q

regulators of formation of the MAC

A

CD59
S protein
HRF or CD59
factor H

55
Q

Membrane protein inhibit formation of the MAC

56
Q

Glycophosphatidylinositol-linked protein expressed on many cell types

57
Q

Incorporate into assembling MACs after the membrane insertion of C5b-8, thereby inhibiting the subsequent addition of C9 molecules

58
Q

Present on normal host cells, where it limits MAC formation, but it is not present on microbes

59
Q

Binding to soluble C5b,6,7 complexes

60
Q

Prevent insertion into cell membranes near the site where the complement cascade was initiated

61
Q

Bind to C8

A

HRF or CD59

62
Q

Inhibits C9 binding

A

HRF or CD59

63
Q

Binds to C3b

64
Q

Facilitates binding of Factor I

65
Q

FACTOR H
Cleaves C3b to _____

A

inactive iC3b

66
Q

FACTOR H
Cleaves C4b to _____

A

inactive fragments

67
Q

Decay Accelerating Factor

68
Q

Immune and rheumatic

A

C1, C2, C3, C4 disorders

69
Q

Recurrent infection (Neisseria)

A

C5, C6, C7, C8 disorders

70
Q

Combined immunodeficiency states

A

C1q disorders

71
Q

Many infections and lupus-like symptoms

A

C1r disorders

72
Q

Systemic Lupus Erythematosus

A

C1s disorder

73
Q

Lupus-like symptoms

A

C4 disorder

74
Q

Increased susceptibility to infection

A

C2 disorder

75
Q

Severe pyogenic infections

A

C3 disorder

76
Q

Recurrent infection of GIT

A

C5 disorder

77
Q

Disseminated gonococcal infections and recurrent Meningococcal meningitis

A

C6, C7, C8 disorder

78
Q

Not more susceptible to disease than other individual in general populations

A

C9 diorder

79
Q

Hereditary angioneurotic oedema

A

C1 inhibitors

80
Q

INACTIVATOR FACTOR 1

81
Q

A multi component triggered enzyme cascade, attracts phagocytic cells to the microbes which engulf them

A

the complement system

82
Q

Complement can be activated by _____ and _____

A

classical and alternative pathway

83
Q

(T/F)
The amount of complement present in the serum
cannot be increased by immunization

84
Q

Complement participates in ________ and ________

A

type II and type III hypersensitivity

85
Q

Several serum complement components are
lowered in many autoimmune diseases such as ______ and ______

A

systemic lupus erythematosus and rheumatoid arthritis

86
Q

(T/F)
Complement mediates immunological membrane damage

87
Q

_______ released during cascade reaction help in amplifying the inflammatory response

A

C fragments

88
Q

It mediate immune adherence

89
Q

It participates in coagulation process

90
Q

Present with early onset SLE, anti-dsDNA less
common, more severe disease, less steroid responsive

A

C1q deficiency

91
Q

Strongest known genetic risk factor for lupus

A

C1q deficiency

92
Q

C4a deficiency, risk factor for SLE (less severity than
sufficient complement) early onset SLE, anti-dsDNA less common

A

C4 deficiency

93
Q

C4B deficiency, with invasive bacterial disease

A

C4 deficiency

94
Q

Most common of the inherited classical complement component deficiencies in Caucasians

A

C2 deficiency

95
Q

most common cause of death in C2 deficiency

96
Q

Most common organisms in C2 deficiency

A

S. pneumoniae and H. influenzae

97
Q

Rarest of the four early component deficiencies

A

C3 deficiency

98
Q

Most severe phenotype

A

C3 deficiency

99
Q

Membranoproliferative glomerulonephritis

A

C3 deficiency

100
Q

Neutrophil dysfunction (abscesses), humoral
deficiencies (sinopulmonary disease), and complement deficiencies (sepsis, meningitis)

A

C3 deficiency

101
Q

Single case has been reported (meningococcemia)

A

factor B deficiency

102
Q

Neisserial infections are the most common manifestation

A

factor D deficiency

103
Q

X-linked complement deficiency

A

properdin deficiency

104
Q

One of the more common complement deficiencies and occurs largely in Caucasians

A

properdin deficiency

105
Q

One or more episodes of meningococcal disease

A

properdin deficiency

106
Q

High fatality rate in contrast to terminal complement component deficiencies

A

properdin deficiency

107
Q

Plasma derived MBL is now being produced by Co-operative Research Centre for Vaccine Technology (CRC-VT)

A

MBL DEFICIENCY THERAPY

108
Q

On phase I safety, tolerability, and pharmacokinetics

A

MBL DEFICIENCY THERAPY

109
Q

● Hereditary angioedema
● Mildly increased susceptibility to infection
● Increased risk of SLE
● Recurrent episodes of angioedema, involvement of airway in absence of anaphylaxis, abdominal episodes, a positive family history, or angioedema arising after trauma
● Type I deficiency, most common (85%) of inherited cases
● Type II deficiency normal production, but dysfunctional protein

A

C1 inhibitor deficiency

110
Q

● Recurrent episodes of hemoglobinuria due to intravascular hemolysis
● Thrombosis occurs for unknown reasons
● Aplastic anemia
● Due to acquired somatic mutations of PIG-A or PIG-M in a clone of bone marrow progenitor cells
● These protein products are required for GPI-anchored proteins and C8-binding proteins which protect hematopoietic cells from complement mediated lysis
● DAF deficiency does not have a hemolytic phenotype
● CD59 is more important

A

PAROXYSMAL NOCTURNAL HEMOGLOBINURIA (PNH)

Immunology & Serology (Lecture) (8 decks)

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