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Immunology Lecture > Complement System > Flashcards

Complement System Flashcards

1
Q

C3a and C5a complements have biological activities as chemoattractants for other immune cells: C3a is for _____ and _____; and C5a is for _____ and _____

A

C3a:
- mast cells
- basophils

C5:
- macrophages
- neutrophils

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2
Q

The complement system functions for each mechanism, except

A

control of infection

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3
Q

Which antibody are commonly involved in the classical pathway?
immunoglobulins

A

IgM and IgG

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4
Q

Which of the following complement proteins initiates the MAC?

A

C5b

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5
Q

The complement system is part of which immune response (IR)?

A

natural IR

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6
Q

The alternative pathway is also known as?

A

C3 convertase pathway

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7
Q

Which of these complements from the pore prior to establishment of MAC?

A

C8 and C9

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8
Q

Which complement system is activated by antigen-antibody complex?

A

Classical Pathway

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9
Q

These complements proteins are part of the activation of classical pathway
3cs

A

C1q
C2
C4

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10
Q

Which of the following describes the terminal complement pathway?

A

Membrane Attack Complex (MAC) for microbial lysis

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11
Q

The alternative pathway functions to

A

Amplify the C3B and further activation leads to formation of C5 convertase of the alternative pathway

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12
Q

Activation of C1 by antibody-binding is correctly called

A

complement fixation

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13
Q

The alternative pathway remains active due to the presence of _______ needed for C3 initiation complex

A

C3(H20)

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14
Q

The alternative pathway commences upon the cleavage and production of which complement protein?

A

C3b

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15
Q

Which two of the following complement proteins comprise C3 convertase of classical pathway?

A

C2a
C4b

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16
Q

These complement proteins comprise C5-convertase complex of the classical pathway
3cs

A

C2a
C3b
C4b

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17
Q

The alternative pathway is activated by which factors

A

Lipopolysaccharides and other LPS present on the surface of invading pathogen

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18
Q

The complement proteins in the serum are generated by means of which enzymes that are part of their respective pathways?

A

protease

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19
Q

Which protein of the Ab is involved in complement activation?

A

Fc region

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20
Q

The classical pathway cascades upon the attachment to Ab of which complement molecule?

A

C1q

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21
Q

essential proteins because it complements the antibacterial activity of some of the antibodies

A

Complements

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22
Q

Complements are given numerical names as

A

C1 to C9, which are 20 including subunits

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23
Q

The concentration of complements is

A

3-4 G/L in the blood.

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24
Q

True or False

Complement makes 10% of the serum proteins.

A

True

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25
Q

This is a function of…

Activation of _____ leads to inflammation and localize the antigen or cause lysis.

A

Complement system

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26
Q

This is a function of…

Once _____ is activated, its components participate in virtually every aspect of the inflammatory response.

A

Complement system

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27
Q

This is a function of…

There is an antimicrobial activity.

A

Complement system

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28
Q

This is a function of…

Serum sickness-like immune reaction.

A

Complement system

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29
Q

This is a function of…

Autoimmune diseases.

A

Complement system

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30
Q

This is a function of…

These are not increased by infection or other antigens.

A

Complement system

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31
Q

This is a function of…

But IL-1 and γ-interferon increase the synthesis.

A

Complement system

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32
Q

Site of Action
cs

A

cell surface or other biological membranes.

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33
Q
  • There are ultrastructural changes in the cell membrane.
  • There are changes in the electrical charges of the cell membrane.
  • There is swelling of the membrane.
  • Ultimately there are circular holes 8-12 nm in diameter.
A

Changes by Activation of Complement

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34
Q
  • The complement may be synthesized in the intestinal epithelium, macrophagic cells, and spleen.
  • C1 is a calcium dependant complex and consists of C1q, C1r, and C1s, this is synthesized in the epithelium of the gastrointestinal and urogenital epithelium
A

Site of Formation

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35
Q

Complement and its Site of Synthesis

Synthesized in Epithelial cells and fibroblasts.

A

C1

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36
Q

Complement and its Site of Synthesis

The liver is the major site of formation.
6cs

A

C3
C4
C6
C7
C8
C9

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37
Q

Complement and its Site of Synthesis

Synthesized by macrophagic cells.

A

C1
C2
C3
C4
C5

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38
Q

factors
Complement and its Site of Synthesis

Synthesized by macrophagic cells.

A

Factor B
Factor D
Factor H
Factor P

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39
Q

Starts forming complement by the second month of pregnancy.

A

Fetus

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40
Q
  • Recognition of antigen and antibody.
  • Enzymatic chain reaction.
  • Formation of membrane attacking complex which leads to cellular destruction
A

Complement activation

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41
Q
  • Complements are present in an inactive form in blood circulation, once activated they give chain reaction like blood coagulation factors.
  • Larger molecule labeled as “b”. It leads to further activation of the chain reaction.
  • A smaller molecule labeled as “a” it promotes inflammation and produces pharmacological action.
  • Further proteolysis gives inactive component labeled as “iC3 b”.
  • Complement is catabolized in the body 1-3% per hour.
A

After Activation Complement is cleaved into

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42
Q

it leads to further activation of the chain reaction.

A

larger molecule

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43
Q

it promotes inflammation and produces pharmacological action

A

smaller molecule

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44
Q

Two Complement pathways

A

Classical pathway
Alternative pathway

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45
Q

Immunological stimuli:

Ag & Ab complex, tissue injury, or aggregated IgG.

Non-immunological stimuli:

CRP, DNA, Trypsin, E. Coli, Salmonella, viruses, endotoxin, and urate crystals.

A

The classical pathway may be activated by:

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46
Q

Immunological stimuli:

aggregated IgA, sometimes IgG.

Non- immunological stimuli:

lipopolysaccharides (endotoxin), Trypsin & trypsin-like enzyme, cobra venom. Parasite & teichoic acid of gram-positive bacteria.

A

Alternative Pathway may be activated by:

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47
Q
  • Lysis of Bacteria, viruses, and cells.
  • Mediate acute inflammation.
  • This leads to the release of histamine.
  • It helps in opsonization and phagocytosis.
  • It has a regulatory role and it regulates acute inflammation in the immune response
A

Activation of Complement leads to:

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48
Q

Vasodilatation at the site of inflammation.

Increase adherence of phagocytic cells to blood vessels endothelium.

It directs movements of phagocytic cells to the area of inflammation.

Ultimately clears of the infection.

A

Various Complement-Proteins lead to:

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49
Q

Physiologic action
Cellular action

A

The outcome of Complement Activation:

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50
Q

Vasodilatation at the site of inflammation.
types of action

A

Physiologic action

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51
Q

Increased vascular permeability.
types of action

A

Physiologic action

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52
Q

Increase adherence of phagocytic cells to blood vessels endothelium.

Hemolysis in the case of RBCs.

Cytolysis.

types of action

A

Cellular action

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53
Q

Recruitment of acute inflammatory cells.
types of action

A

Cellular action

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54
Q

It directs movements of phagocytic cells to the area of inflammation.
types of action

A

Cellular action

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55
Q

Produce inflammatory mediators.
types of action

A

Cellular action

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56
Q

type of action
Opsonization of the pathogens
types of action

A

Cellular action

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57
Q

Ultimately clears of the infection.

Ultimately killing of pathogens.

A

Opsonization of the pathogens of Cellular Action

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58
Q

Various cell types express surface membrane glycoproteins that react with one or more of the fragments of C3 produced during complement activation and degradation.

A

Complement Receptors

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59
Q

important in increasing phagocytosis and an important factor present on the RBCs.

A

Complement receptor 1 (CR1)

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60
Q

CD molecule:
CD5

Specificity for the receptor:
C3b

Distribution on the cells: RBCs
Polys
Monocytes
B-lymphocytes
Dendritic cells
Glomerular visceral epithelial cell

Main functions
Promote Phagocytosis
Immune complex transport
Immune adhesion
Secondary Epstein Barr virus receptor

A

CR1 (Complement receptor 1)

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61
Q

cr?

CD molecule:
CD21

Specificity for the receptor:
C3d

Distribution on the cells: B-lymphocytes

Main functions:
B-cell coactivator
CD23 receptor
Epstein Barr virus receptor

A

CR2 (Complete receptor 2)

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62
Q

CD molecule:
CD11b and CD18

Specificity for the receptor:
iC3b

Distribution on the cells: Monocytes
Polys
NK cells

Main functions:
Polys adherence
Phagocytosis of iC3b bound particles

A

CR3 (Macrophage-1-antigen)

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63
Q

In the classic pathway antigen and antibody complex is recognized by the complement _______ and it starts a chain reaction by stimulating C1s and C1r which will stimulate C4 and C2. Then there is the stimulation of C3 C5 C6, 7, and ultimately C9.

A

C1q

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64
Q

The activation of complement is not in sequence from C1 to C9, but this is

A

C1, C4, C2, C3, C5, C6, C7, C8 and C9

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65
Q

the recognition unite and it recognizes the Ag-Ab complex and then activates C1r

A

C1q

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66
Q

molecule has a stable binding to the cell membrane (efficiency is <10%)

A

C4b

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67
Q

Clusters of C3b are activated and bound near the C4bC2b complex

A

C3b

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68
Q

acts as a C5 convertase and cleaves C5 into C5a and C5b.

A

C4b C2b C3b

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69
Q

fixation and is the beginning of the membrane attack complex.

A

C5b

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70
Q

is highly lipophilic and binds to the membrane where it acts high-affinity receptors for C8.
three cs

A

C5b
C6
C7

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71
Q

has three chains α, β, and γ where γ-chains insert into the membrane.

A

C8

72
Q

polymerizes C9 forming tubule the MAC (membrane attacking complex), which gives rise to hole formation in the cell-membrane Like drill machine.
four cs

A

C5b
C6
C7
C8

73
Q

directly binds to the immunoglobulin molecule.

A

C1q

74
Q

do not bind the immunoglobulin but leads to the subsequent activation of C3.
2 cs
1r
1s

A

C1r and C1s

75
Q

only attaches to subclasses of IgG and IgM

A

C1q

76
Q

single molecule is able to fic C1 but IgG needs two molecules.

A

IgM

77
Q

is functionally multivalent for to attach to the complement fixation sites of immunoglobulin.

A

C1q

78
Q

are similar in structure, where ____ forms dimers and ____ binds to ____.

A

C1r and C1s

79
Q

both bind to C1q in the presence of Ca++.

A

C1q

80
Q

the only substrate for C1r.

A

C1s

81
Q

cleaves C1S (C1S–).

A

C1r-

82
Q

C1s also cleaves

A

C2 to C2a and C2b

83
Q

The control mechanism for the activity of C1s is a _______, which will control the C1s for un-controlled activation of C4 and C2.

A

C1-proteinase inhibitor

84
Q

has the ability to disintegrate the membrane-bound C4b.

A

C3b esterase inhibitor

85
Q

act as C3-convertase and cleaves C3 to C3a and C3b

2cs

A

C4b and C2b

86
Q

two cs
will activate the C3 molecule into C3a anaphylatoxin and C3b.

A

C4b
C2b

87
Q

forms an opsonic macromolecular coat on the target cells and makes it susceptible to immune adherence by the C3b receptor on the phagocytic cells.
three cs

A

C4b
C2b
C3b

88
Q

Only a ___ molecule combines with C4bC2b to form the final proteolytic complex complement pathway.

A

C3b

89
Q

binds to C6 and make a labile reactive site for C7.

A

C5b

90
Q

It is evaluated in the serum.

It is needed in the first reaction of complement where it will lead to activation of C4 and C2.

A

C1q

91
Q

It takes part in the activation of C3 with the help of C4.

A

C2 and C2a

92
Q

It increases vascular permeability.

A

C2 and C2a

93
Q

It causes contraction of smooth muscles.

A

C2 and C2a

94
Q

Some say that functions are unknown.

A

C2 and C2a

95
Q

It is a weak anaphylatoxin and weak mediator of Inflammation.

A

C4a

96
Q

It is a strong anaphylatoxin.

A

C3a

97
Q

It leads to an increase in vascular permeability and smooth muscle contraction.
not ctwo

A

C3a

98
Q

This leads to the release of vasoactive amines.

A

C3a

99
Q

Leads to the release of lysosomal enzyme.
It is chemotactic.

A

C3a

100
Q

Functions just like C3a.

A

C5a

101
Q

It increases neutrophil activity.

A

C5a

102
Q

More potent chemotactic factor than C3a.

A

C5a

103
Q

Activated by the C5b and attach to C7.

A

C6

104
Q

These are C3a, C5a, and C4a.

A

Anaphylatoxin

105
Q

these directly activate mast cells and basophils, through their receptor for C5a, and lesser extent C3a.

A

Anaphylatoxin

106
Q

has the highest biologic activity.

A

C5a

107
Q

acts with C5a to activate mast cells, recruit antibody, complement, phagocytes, and increase the tissue fluid in that area.

A

C3a

108
Q

has the least anaphylactic activity.

A

C4

109
Q

Binding to Ag-Ab complex (Recognition unit)

A

C1q

110
Q

Activating enzymes

A

C1r, C1s, C2b, Bb & D

111
Q

two cs
Membrane binding proteins and Opsonin

A

C3b & C4b

112
Q

three cs
Mediate inflammation

A

C5a, C3a, C4a

113
Q

Membrane-attacking complex

A

C5b6789

114
Q

It is a glycoprotein and also known as C1 esterase. It destroys C1r, C1s.

A

C1-inhibitor

115
Q

It is proteolytic enzymes, it cleaves C3b into iC3b (inactive form). It also destroys C4b.
what factor?

A

The factor I

116
Q

Prevents binding of C5, 6, 7 to the membrane.

A

Vitronectin (S-protein)

117
Q

prevents activation of C4.

A

Decay Accelerating Factor (DAF)

118
Q

Prevents activation of C4.

A

C4 binding protein

119
Q

what factor?
It binds C3b and accelerates the destructive action of factor I.

A

Factor H

120
Q

This is a primitive defense system. In this pathway, there is a bypass of C1, 4, 2 and there is direct stimulation of C3.

A

ALTERNATIVE PATHWAY

121
Q

This is predominantly a non-antibody initiated pathway.

A

ALTERNATIVE PATHWAY

122
Q

activator of the alternative complement pathway

A

Polysaccharides complex from the surface yeast cells.

Bacterial polysaccharides and endotoxin.

Aggregated immunoglobulins IgG2, IgA, and IgE.

Zymosan.

Inulin.

123
Q

considered the counterpart of the C2a of the classical pathway.

A

C3a

124
Q

of the classical pathway resembles factor B of the alternative pathway.

A

C2

125
Q

no role of C1, C2, and C4, but the alternative pathways have different protein which stimulates directly

A

C3

126
Q

Factor C3b and factor B combine to form ___,___
which is then converted into C3 convertase (C3bBb)

A

C3b, B

127
Q

a glycine richα-2-globulin believed to be physiologically inactive through the action of factor D.
factor

A

Factor Ba

128
Q

can convert more C3 to C3b, in turn, it binds more factor B.

A

C3b, Bb complex

129
Q

The complement (C) system is part of the immune system called the

A

innate immune system.

130
Q

This test can be used to diagnose various diseases e.g Pneumococcal pneumonia, syphilis and etc.
With the help of this test, one can quantitate antigen or antibody.
This test was very famous for the diagnosis of syphilis.

A

Complement fixation test

131
Q

This test may be manipulated by making dilution of serum or complement or one can have known antibody and unknown antigen or vice versa. Even the titer of antibody or concentration of complement may be estimated by serial dilution.

A

Complement fixation test

132
Q

This test is used to find Unknown Antibody or Antigen

A

Complement fixation test

133
Q

The basic principle is its activity which leads to hemolysis of RBC. In this test, we need:

Serum of the patients.
Complement
Indicator system which consists of antibody-coated RBC.
Known antigen.

A

Complement fixation test

134
Q

Diseases caused by the complement deficiency
C1s

A

SLE
Angioedema

135
Q

Diseases caused by the complement deficiency
C1r

A

Glomerulonephritis
Chronic infection
SLE
Dermatomyositis
Vasculitis
Necrotizing skin lesion
Arthritis

136
Q

Diseases caused by the complement deficiency
C1q

A

SLE
Decreased secondary to agammaglobulinemia
C2

137
Q

Diseases caused by the complement deficiency
C2

A

Recurrent pyogenic infection
SLE
Membranoproliferative glomerulonephritis
Discoid lupus erythematosus
Dermatitis herpetiformis
Dermatomyositis
Synovitis
Purpura
Hodgkin’s disease
Chronic lymphocytic leukemia
Polymyositis
C3

138
Q

Diseases caused by the complement deficiency
C3

A

Recurrent pyogenic infection
SLE
Arthritis
Skin rash

139
Q

Diseases caused by the complement deficiency
C3b inactivator

A

Recurrent pyogenic infection
Urticaria

140
Q

Diseases caused by the complement deficiency
C4

A

SLE
Vasculitis
Dermatomyositis like syndrome

141
Q

Diseases caused by the complement deficiency
C5

A

Recurrent infection (Neisserai)
SLE

142
Q

Diseases caused by the complement deficiency
C6

A

Gonorrheal infection
Meningococcal infection
SLE
Scleroderma
Vasculitis
Raynaud’s phenomenon

143
Q

Diseases caused by the complement deficiency
C7

A

Raynaud’s disease
Renal disease
Neisseria infection
SLE
Vasculitis
Scleroderma

144
Q

Diseases caused by the complement deficiency
C8

A

Glomerulonephritis
SLE
Neisseria infection
Xeroderma pigmentosa

145
Q

Decreased Level Of Complement (Deficiency Of Complements):

A

Autoimmune diseases
Infectious diseases
Deficiency of controlling proteins

146
Q

what kind of disease?
SLE.
Rheumatoid arthritis.
Systemic vasculitis.
Essential mixed cryoglobulinemia.

A

Autoimmune diseases

147
Q

what kind of disease?
Arterioventricular shunts with infection.
Subacute bacterial endocarditis.
Gram-negative sepsis.
Pneumococcal sepsis.
Viral hepatitis B leading to viremia.
Viremia in measles.
Malarial parasite infestation.

A

Infectious diseases

148
Q

These are quite uncommon primary immune deficiency <2%.
The factor H deficiency.
The factor I deficiency.
Hereditary angioedema (C1 inhibitor deficiency).

A

Deficiency of controlling proteins

149
Q

Inflammatory process.
Trauma.
Myocardial infarction.
In acute illnesses where complement raised as acute-phase proteins.

A

Raised Level Of Complement:

150
Q

Diseases associated with complement deficiency
C1s deficiency
C4 deficiency

A

SLE

151
Q

Diseases associated with complement deficiency
C1q deficiency

A

SLE, Nephritis & hypogammaglobulinemia

152
Q

Diseases associated with complement deficiency
Renal diseases, SLE, recurrent infection, and Rheumatoid arthritis

A

C1r deficiency

153
Q

Diseases associated with complement deficiency
Recurrent infections (pyogenic)

A

C3 deficiency

154
Q

Diseases associated with complement deficiency
Recurrent infections + Gonococcal infections and SLE

A

C5 deficiency

155
Q

Diseases associated with complement deficiency
Recurrent infections + Meningococcal infection

A

C6 deficiency

156
Q

Diseases associated with complement deficiency\
Recurrent infections + Glomerulonephritis

A

C7 deficiency

157
Q

Diseases associated with complement deficiency
Recurrent infections + Gonococcal & Meningococcal infections

A

C8 deficiency

158
Q

Binds to pathogen surface.

Binds factor B for cleavage by D.

A

C3b

159
Q

It is a C3 convertase.

A

C3bBb

160
Q

It is a C5 convertase.

A

C3b2Bb

161
Q

It is a small fragment and function is unknown

A

Ba

162
Q

It is an active enzyme and C3 convertase.

A

Bb

163
Q

factor
Plasma serine protease cleaves factor B when it is bound To C3b to Ba and Bb.

A

Factor D

164
Q

are certain substances, which enhance and give positive regulation of the alternative pathways:

Factor P (Properdin).
Cobra Venom Factor (CoVF):- This complexes with Bb (CoVFBb) which acts as C3/C5 convertase. It is resistant to factor H & I.

A

Positive Regulators for Alternative Pathways

165
Q

Inhibitors of Alternative Pathways

A

Factor H which binds to C3b.

166
Q

It present on Mast cells and Basophils
not c3

A

C1q

167
Q

Present on Mast cells and Basophils.
Receptors identified on Neutrophil, Monocytes, B, and Null cells.

A

C3a and C5a Receptors

168
Q

Receptors identified on Neutrophil, Monocytes, B, and Null cells.

A

C3b

169
Q

Present on phagocytic cells, lymphocytes, and RBC.

A

C4b

170
Q

Virus neutralization.

A

C1 and C4

171
Q

Immune adherence, phagocytosis & take part in Arthus reaction.

A

C3b

172
Q

Anaphylatoxin

A

C3a, C5a

173
Q

Chemotaxis
4 cs

A

C3a, C5a, and C6 C7

174
Q

Lysis
-to-

A

C5 to C9

175
Q

Cytotoxic action

A

C8 and C9

Immunology Lecture (1 decks)

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