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IMMUNOLOGY AND SEROLOGY LECTURE > C4 > Flashcards

C4 Flashcards

1
Q
  • coined the term “complement” because it complements the action of antibody in destroying microorganisms.
A

Paul Ehrlich

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2
Q

Heat labile series of more than 30 plasma proteins

A

complement”

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3
Q

named with a (?) followed by a (?)

A

capital C

number

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4
Q
  • results from the cleavage of a larger precursor by a protease
A

small letter

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5
Q

complement” example

A

C3a/ C3b

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6
Q
  • designated as b
A

Larger fragment

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7
Q
  • designated as a
A

Smaller fragment

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8
Q

Exception:

A

C2 fragments

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9
Q

Larger- (?), smaller fragment- (?)

A

C2a

C2b

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10
Q

Proteins and glycoproteins synthesized mainly by liver

A

COMPONENTS

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11
Q

Most circulate in the serum functionally inactive forms

A

COMPONENTS

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12
Q

Produces a cascade phenomenon where the product of one reaction is the enzymatic catalyst of the next

A

COMPONENTS

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13
Q

(?) soluble and cell-bound proteins

A

30

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14
Q

FUNCTIONS OF COMPLEMENT

A
  1. Lysis of cells, bacteria and viruses
  2. Opsonization
  3. Triggers specific cell functions, inflammation and secretion of immunoregulatory molecules
  4. Immune clearance: removal of immune complexes and deposition in the spleen and liver
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15
Q

Biological Functions

A
  1. Anaphylatoxin
  2. Increase Capillary Permeability
  3. Chemotaxis
  4. Virus neutralization
  5. Opsonization
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16
Q

Main Complement Component Involved Opsonization

A

C3b

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17
Q

Main Complement Component Involved Anaphylatoxin

A

C3a, C4a, C5a

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18
Q

Main Complement Component Involved Increase Capillary Permeability

A

Role of C2b fragment

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19
Q

Main Complement Component Involved Chemotaxis

A

C5a

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20
Q

Main Complement Component Involved Virus neutralization

A

C4

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21
Q

They bind to receptors on mast cells and basophils

A

Anaphylatoxin

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22
Q

Induce degranulation and release of influx mediators including histamine

A

Anaphylatoxin

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23
Q

small peptide that causes increased vascular permeability, contraction of smooth muscle, and release of histamine from basophils and mast cells.

A

Anaphylatoxin

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24
Q

Can lead to edema if complement is not controlled

A

Increase Capillary Permeability

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25
Q

Attract cells and play important role in recruitment of cells to an influx site

A

C5a

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26
Q

Enhances neutralization of viruses by homologous antibodies

A

C4

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27
Q

C3b on particles such as bacteria or an Ab-Ab complex promotes the attachment and ultimate ingestion of the particles.

A

C3b

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28
Q

CLASSICAL Initiated by:

A

Antigen-antibody complex

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29
Q

ALTERNATE/ALTERNATIVE/PROPERDIN Initiated by:

A
  1. Aggregates of IgA
  2. Yeast cell or zymogen
  3. CVF
  4. LPS
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30
Q

LECTIN Initiated by:

A

With mannose and other similar sugars in the cell wall

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31
Q

Recognition event which will initiate complement cascade

A

INITIATION PHASE

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32
Q

Classical and alternate pathway differ at this phase

A

INITIATION PHASE

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33
Q

Activation of early components culminate in activation of C3 which is the critical component

A

AMPLIFICATION/ ACTIVATION PHASE

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34
Q

Classical and alternate pathway differ at this phase

A

AMPLIFICATION/ ACTIVATION PHASE

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35
Q

Culminates in target cell lysis

A

MEMBRANE ATTACK PHASE

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36
Q

Classical and alternate pathway is the same at this phase

A

MEMBRANE ATTACK PHASE

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37
Q

Phases of Complement Activation

A
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38
Q

Initiation of Pathways

A
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39
Q

Activation of the Complement

A
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40
Q

Bonding of C1 complex (C1q, C1r, C1s) to antibodies bound to an antigen on the surface of a bacterial cell.

A

Classic Pathway

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41
Q

Contact with a foreign surface such as the polysaccharide coating of a microorganism

A

Alternative

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42
Q

Covalent bonding of a small amount of C3b to hydroxyl groups on cell surface carbohydrates and proteins.

A

Alternative

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43
Q

Activated by low-grade cleavage of C3 in plasma

A

Alternative

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44
Q

Binding of the complex of mannose binding lectin and associated serine proteases (MASP1 and MASP2) to arrays of mannose groups on the surface of a bacterial cell.

A

Mannose Binding

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45
Q

Major effector mechanisms of antibody-mediated immunity.

A

CLASSICAL PATHWAY

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46
Q

CLASSICAL PATHWAY
Principal components:

A

C1-C9

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47
Q

CLASSICAL PATHWAY
Activation:

A

C1, 4, 2, 3, 5, 6, 7, 8 and 9

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48
Q

present in the plasma in the largest quantities

A

C3

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49
Q

fixation of (?) is the major quantitative reaction of the complement cascade

A

C3

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50
Q

CLASSICAL PATHWAY
3 major stages:

A
  1. Recognition
  2. Amplification of proteolytic complement cascade
  3. Membrane attack complex (MAC)
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51
Q

Begins with the formation of soluble antigen-antibody complexes or with binding of antibody to antigen on a suitable target such as a bacterial cell

A

CLASSICAL PATHWAY

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52
Q

IgM or IgG

A

CLASSICAL PATHWAY

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53
Q

Ag-Ab-IgM : conformational change in Fc : exposing a binding site for C1

A

CLASSICAL PATHWAY

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54
Q

is the recognition unit that binds to the FC portion of two antibody molecules

A

C1qrs

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55
Q

C1s is activated and cleaves C4 and C2 to form (?), which is known as C3 convertase.

A

C4b2a

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56
Q

C3 convertase cleaves C3 to form (?), known as C5 convertase.

A

C4b2a3b

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57
Q

The combination of (?) is the activation unit.

A

C4b2a3b

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58
Q

(?) cleaves C5.

A

C5 convertase

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59
Q

C5b attracts (?), which bind together, forming the membrane attack complex.

A

C6, C7, C8, and C9

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60
Q

(?) polymerizes to cause lysis of the target cell.

A

C9

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61
Q

Antibody is not required

A

ALTERNATIVE PATHWAY

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62
Q

Innate immunity

A

ALTERNATIVE PATHWAY

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63
Q

ALTERNATIVE PATHWAY
4 serum proteins:

A

C3, factor B, factor D and properdin

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64
Q

Initiated by cell-surface constituents that are foreign to the host (gram + and gram – bacterial cell walls)

A

ALTERNATIVE PATHWAY

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65
Q

Factors capable of activating the alternative pathway

A

✓ Inulin
✓ Zymosan
✓ Bacterial polysaccharides and endotoxins
✓ Aggregated IgG2, IgA and IgE

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66
Q

: proteins that recognize and bind to specific carbohydrate targets

A

Lectins

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67
Q

After initiation proceeds thru action of C4 and C2 to produce C5 convertase

A

MANNOSE BINDING LECTIN PATHWAY

68
Q

Activated by binding of mannose-binding lectin to mannose residues on glycoproteins or carbohydrates on the surface of microorganisms such as Salmonella, Listeria, Neisseria, Cryptococcus and Candida.

A

MANNOSE BINDING LECTIN PATHWAY

69
Q

The binding of (?) to two antibody molecules activates the classical pathway, while the alternative pathway is started by hydrolysis of C3.

A

C1qrs

70
Q

The (?) is triggered by binding of MBP to mannose on bacterial cell walls.

A

lectin pathway

71
Q

(?) bind to form an activated C1-like complex.

A

MASP-1, MASP-2, and MASP- 3

72
Q

(?) cleaves C2 and C4 and proceeds like the classical pathway.

A

MASP-2

73
Q

(?) operate in the alternative pathway.

A

Factor B and factor D

74
Q

While C3 convertase is formed differently in each pathway, (?) is a key component in each one.

A

C3

75
Q

The C5 convertase in the alternative pathway consists of (?).

A

C3bBb3bP

76
Q

In the classical pathway, C5 convertase is made up of (?).

A

C4b2a3b

77
Q

After (?) is cleaved, the pathway is common to all.

A

C5

78
Q

3 pathways: active C5 convertase to cleave C5 — [?] (initiates the final steps to form MAC)

A

C5a and C5b

79
Q

Forms a large channel through the membrane of the target cell enabling ions and small molecules to diffuse freely across the membrane.

A

MEMBRANE ATTACK COMPLEX

80
Q

Molecular wt.
410

A

C1q

81
Q

Molecular wt.
85

A

C1r

C1s

82
Q

Molecular wt.
205

A

C4

83
Q

Molecular wt.
102

A

C2

84
Q

Molecular wt.
190

A

C3

C5

85
Q

Molecular wt.
110

A

C6

86
Q

Molecular wt.
100

A

C7

87
Q

Molecular wt.
150

A

C8

88
Q

Molecular wt.
70

A

C9

89
Q

Conc.(ug/mL)
150

A

C1q

90
Q

Conc.(ug/mL)
50

A

C1r

C1s

91
Q

Conc.(ug/mL)
300-600

A

C4

92
Q

Conc.(ug/mL)
25

A

C2

93
Q

Conc.(ug/mL)
1200

A

C3

94
Q

Conc.(ug/mL)
80

A

C5

95
Q

Conc.(ug/mL)
45

A

C6

96
Q

Conc.(ug/mL)
90

A

C7

97
Q

Conc.(ug/mL)
55

A

C8

98
Q

Conc.(ug/mL)
60

A

C9

99
Q

Binds to Fc region of IgM and IgG

A

C1q

100
Q

Activates C1s

A

C1r

101
Q

Cleaves C4 and C2

A

C1s

102
Q

Part of C3 convertase (C4b)

A

C4

103
Q

Binds to C4b—forms C3 convertase

A

C2

104
Q

Key intermediate in all pathways

A

C3

105
Q

Initiates membrane attack complex

A

C5

106
Q

Binds to C5b in MAC

A

C6

107
Q

Binds to C5bC6 in MAC

A

C7

108
Q

Starts pore formation on membrane

A

C8

109
Q

Polymerizes to cause cell lysis

A

C9

110
Q

Molecular wt.
93

A

Factor B

111
Q

Conc.(ug/mL)
200

A

Factor B

112
Q

Binds to C3b to form C3 convertase

A

Factor B

113
Q

Molecular wt.
24

A

Factor D

114
Q

Conc.(ug/mL)
2

A

Factor D

115
Q

Cleaves factor B

A

Factor D

116
Q

Molecular wt.
55

A

Properdin

117
Q

Conc.(ug/mL)
15-25

A

Properdin

118
Q

Stabilizes C3bBb–C3 convertase

A

Properdin

119
Q

Molecular wt.
200-600

A

MBL

120
Q

Conc.(ug/mL)
0.0002-10

A

MBL

121
Q

Binds to mannose

A

MBL

122
Q

Molecular wt.
93

A

MASP-1

123
Q

Conc.(ug/mL)
1.5-12

A

MASP-1

124
Q

Unknown

A

MASP-1

125
Q

Molecular wt.
76

A

MASP-2

126
Q

Conc.(ug/mL)
Unknown

A

MASP-2

127
Q

Cleaves C4 and C2

A

MASP-2

128
Q

Lupus like syndrome; recurrent infections

A

C1 (q, r, or s)

129
Q

Lupus like syndrome; recurrent infections; atherosclerosis

A

C2

130
Q

Severe recurrent infections; glomerulonephritis

A

C3

131
Q

Lupus like syndrome

A

C4

132
Q

Neisseria infections

A

C5-C8

133
Q

No known disease association

A

C9

134
Q

Hereditary angioedema

A

C1INH

135
Q

Paroxysmal nocturnal hemoglobinuria

A

DAF

136
Q

Paroxysmal nocturnal hemoglobinuria

A

MIRL

137
Q

Recurrent pyogenic infections

A

Factor H or factor I

138
Q

Pneumococcal disease, sepsis, Neisseria infections

A

MBL

139
Q

Neisseria infections

A

Properdin

140
Q

Pneumococcal diseases

A

MASP-2

141
Q

associated with inflammatory conditions, trauma, or acute illness

A

INCREASED COMPLEMENT LEVELS

142
Q

Limited clinical significance

A

INCREASED COMPLEMENT LEVELS

143
Q

Low levels of complement suggest one of the following biological effects:

A

• Complement has been excessively activated recently.
• Complement is currently being consumed.
• A single complement component is absent because of a genetic defect.

144
Q

result from the complexing of IgG or IgM antibodies capable of activating complement

A

HYPOCOMPLEMENTEMIA

145
Q

associated with diseases that give rise to circulating immune complexes.

A

HYPOCOMPLEMENTEMIA

146
Q

The (?) is a series of more than 30 proteins normally found in serum that play a major role in phagocytosis and clearance of foreign antigens from the body.

A

complement system

147
Q

While the end product of complement activation is lysis, other important events, such as (?) of monocytes and neutrophils take place along the way to enhance host defense mechanisms.

A

opsonization, increase in vascular permeability, and chemotaxis

148
Q

Most of the proteins of the complement system are inactive enzyme precursors, or (?), that are converted to active enzymes in a very precise order.

A

zymogens

149
Q

One means of activation is the (?), which is triggered by antigen–antibody combination and involves nine of the proteins.

A

classical pathway

150
Q

(?) plays a major role in several disease states.

A

Complement

151
Q

Decreased complement levels or a decline in lytic activity can indicate either (?)

A

hereditary deficiencies or extreme activation of the system

152
Q

(?) are two conditions that result from missing or very low production of certain regulators.

A

Paroxysmal nocturnal hemoglobinuria and hereditary angioedema

153
Q

Deficiencies of some components, especially that of C3, may cause an increased risk of (?) due to a lack of clearance of immune complexes.

A

lifethreatening infection or glomerulonephritis

154
Q

Several laboratory assays have been devised to detect (?).

A

abnormal complement levels

155
Q

One of these, the (?), uses 50 percent lysis of a standard concentration of antibody-sensitized sheep erythrocytes as an end point.

A

CH50 hemolytic assay

156
Q

This measures the presence of all proteins involved in the classical pathway.

A

CH50 hemolytic assay

157
Q

A similar assay, the (?), measures the functioning of the alternative pathway.

A

AH50 assay

158
Q

Other assays using (?) measure levels of individual components.

A

RID or ELISA techniques

159
Q

(?) is essential to ensure correct interpretation of laboratory testing.

A

Proper handling of specimens

160
Q

(?) use complement as a reagent to detect the presence of antigen or antibody.

A

Complement fixation tests

161
Q

(?) are allowed to combine with a measured amount of complement.

A

Antigen and antibody

162
Q

Then indicator (?) are added.

A

sheep red blood cells

163
Q

These are coated with (?) (antisheep cell antibody), and if complement has not been tied up in the first reaction, then lysis of the cells occurs.

A

hemolysin

164
Q

Thus, (?) is a negative test, indicating that either antigen or antibody was not present.

A

lysis

165
Q

As in all complement testing, the use of (?) is necessary for accurate results.

A

standards and control

IMMUNOLOGY AND SEROLOGY LECTURE (12 decks)

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