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Block 6 Week 1 Colt > Complement System - Hunter > Flashcards

Complement System - Hunter Flashcards

1
Q

complement system is involved in (innate/adaptive) immunity

A

innate and adaptive!

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2
Q

complement proteins are (constitutively/variably) expressed

A

constitutively

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3
Q

where are complement proteins expressed?

A

serum and on cell surfaces

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4
Q

the complement system is important in eliminated immune (blank)

A

complexes

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5
Q

genetic defects in the complement system increase the risk for infecions of (blank) bacteria and can precipitate immune (blanks)

A

pyogenic bacteria; immune complexes

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6
Q

the complement system shares features with what two other systems?

A

coagulation and kinin systems

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7
Q

complement functions by cleaving (blanks) into active enzymes

A

zymogens

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8
Q

one protease cleaves and activates many molecues of the next component, (blanking) the response to bugs

A

amplifying

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9
Q

what are the major functions of complement?

A
  1. opsonization
  2. inflammation and chemotaxis and activation of immune cells
  3. clearance of immune complexes
  4. form pores and causes lysis of pathogens
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10
Q

what does a capital letter indicate on a complement protein?

A

that it is a whole protein

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11
Q

what does a lower case letter indicate on a complement protein?

A

that it is a cleavage fragment

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12
Q

what are the two exceptions to the lower case letter rule?

A

C1r and C1s

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13
Q

what is the letter for the small fragment and what is it for the big fragment?

A

a for small, b for big; BUT C2b is often the small one

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14
Q

what does “i” before a name indicate?

A

that it is the inactive form, BUT CAN STILL BIND TO C RECEPTORS

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15
Q

what is the order of activation in the classical pathway?

A 
C1
C4
C2
C3
C5-9
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16
Q

What complement protein is involved in binding to Ag:Ab complexes and pathogen surfaces?

A

C1q

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17
Q

What complement protein is involved in binding to CHO structures like mannos or GlcNAc on micbrobial surfaces?

A
  1. MBL
  2. Ficolins
  3. C1q
  4. properdin (factor P)
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18
Q

What complement protein is involved in activating enzymes?

A
  1. C1r
  2. C1s
  3. C2a
  4. Bb
  5. D
  6. MASP-2
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19
Q

What complement protein is involved in membrane binding proteins and opsonins?

A
  1. C4b

2. C3b

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20
Q

What complement protein is involved in peptide mediators of inflammation?

A
  1. C5a
  2. C3a
  3. C4a
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21
Q

What complement protein is involved in membrane attack complexes?

A
  1. C5a

2. C6-9

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22
Q

What complement proteins are complement receptors?

A

CR1-4 and CRIG

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23
Q

What are the complement regulatory proteins?

A 
C1INH
C4BP
CR1
MCP
DAF
H
I
P
CD59
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24
Q

(blank) is a pattern recognition receptor that can bind to repeating molecular motifs on pathogens like bacterial porins and LPS

A

C1q

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25
Q

(blank) also binds IgM, IgG, or CRP deposited on pathogen surfaces

A

C1q

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26
Q

What other two proteins is C1q associated with to form the complete C1 complex?

A

C1r and C1s

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27
Q

What structural protein makes a large tube at the top of the C1 complex?

A

collagen

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28
Q

After C1q binds to a pathogen, (blank) becomes an active serine protease

A

C1s

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29
Q

When activated, C1s will cleave (blank) into small and large fragments (blank-a/b)

A

C4 into C4a/b

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30
Q

If C4b is not immediately hydrolyzed, how does it bind to the pathogen surface?

A

covalently!

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31
Q

After cleaving C4, what next does C1q do?

A

It cleaves C2, which then associates with C4b

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32
Q

The C4b2a complex is the (blank) of the classical pathway

A

C3 convertase

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33
Q

What is the function of C3 convertase?

A

Cleaves C3 into C3b that binds covalently to the pathogen; C3a floats away

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34
Q

After C3 convertase activity, what is the new total complex called?

A

C4b2a3b

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35
Q

Thousands of (blank) C3b molecules are deposited on the pathogen surface when it is cleaved by C3 convertase

A

opsonic

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36
Q

C3b and C4b are highly reactive and (blanks) quickly if no bound to pathogen surfaces

A

hydrolyzes

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37
Q

what holds together the a and b portions of C3?

A

disulfide bonds

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38
Q

Does the a or b chain of C3 contain TED?

A

alpha

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39
Q

What is the type of bond within TED that allows C3b to bind to the pathogen surface?

A

thioester

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40
Q

Pathogens opsonized by C3b are endocytosed and killed by (blank) cells

A

phagocytic cells

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41
Q

what three phagocytic cells have receptors for C3 and its breakdown products?

A

Macrophages
neutrophils
dendritic cells

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42
Q

What is the MOST IMPORTANT INNATE defense against extracellular pathogens?

A

C3b-mediated opsonization and killing

43
Q

What can the CR3 receptor bind besides C3?

A

iC3b

44
Q

Complement activation promotes clearing of immune (blanks)

A

complexes

45
Q

When clearing immune complexes, what happens when C1q binds to the complex?

A

C4b and C3b molecules are deposited onto the complex

46
Q

To what receptor do immune complexes bind on RBCs?

A

CR1

47
Q

Which complement proteins bind the CR1 receptor on RBCs?

A

C4b and C3b strangely enough

48
Q

Where are immune complexes stripped from the RBCs and degraded?

A

spleen and liver

49
Q

Deficiencies in which complements can lead to immune complex diseases such as SLE?

A

C1, C4, or C2

50
Q

What receptor does the immune complex bind in the spleen to transfer it from the RBC to the phagocytic cell?

A

FcR

51
Q

(blank) binds mannose and other common bacterial sugars

A

Mannose binding lectin

52
Q

(blanks) L-, M-, and H- bind microbial oligosaccharides like GlcNac

A

Ficolins

53
Q

MBL and ficolins are homologous to what complement protein?

A

C1q

54
Q

MBL-associated serine proteases (MASP-1/2) are equal to what complement protein?

A

C1r/s

55
Q

T/F: the MBL pathway forms the C3 convertase (C4b2a)

A

True

56
Q

The Alternate pathway can (amplify/dampen) the classical and lectin pathways

A

amplify

57
Q

(blank) protein deposited on the pathogen surface by the classical or lectin pathway can engage the alt. pathway

A

C3b

58
Q

Factor (blank) binds to C3B, and is then cleaved to Bb by factor (blank)

A

Factor B, Factor D

59
Q

What makes up the C3 convertase in the alternate pathway?

A

C3bBb

60
Q

C3a is also known as the potent (blank)

A

anaphylatoxin

61
Q

C3bBb is stabilized by (blank)

A

properdin aka factor P

62
Q

What are the two C5 convertases?

A

C4b2a3b

C3b2Bb

63
Q

What is the function of the C5 convertase?

A

cleave C5 into C5b and C5a

64
Q

C5b triggers the assembly of (blank)

A

THE MEMBRANE ATTACK COMPLEX

65
Q

C5a is also known as a potent (blank)

A

anaphylatoxin

66
Q

Which anaphylatoxin has the highest specific biologic availability?

A

C5a

67
Q

Which anaphylatoxin acts directly on neutrophils and monocytes to speed up phagocytosis of pathogens?

A

C5a

68
Q

What are the functions of C3a?

A

activate mast cells, recruit Ab, complement, and phagocytic cells via chemotaxis and increase fluid in the tissues

69
Q

What is the least active anaphylatoxin?

A

C4a

70
Q

Overexpression of anaphylatoxin can cause (blank)

A

systemic anaphylaxis

71
Q

which proteins are involved in forming the memrane attack complex?

A

C5b

C6-9

72
Q

Describe the process of the MAC formation?

A
  1. C5b binds to C6 and C7
  2. C8 binds to C5b67 and INSERTS INTO THE MEMBRANE
  3. C9 binds and polymerizes to form a pore
73
Q

What bugs are routinely killed used the MAC?

A

Neisseria miningitidis or gonorrheae

74
Q

Deficiencies in the classical pathway lead to (blank)

A

immune-complex disease

75
Q

Deficiencies in the MBL pathway leads to (blank)

A

childhood pyogenic bacterial infections

76
Q

Deficiencies in the alternate pathway leads to (blank)

A

infections with pyogenic bacteria and Neisseria BUT NO IMMUNE COMPLEX

77
Q

T/F: when complement is activated by pathogens, some components can become depleted

A

True

78
Q

use CH50 to screen for the (bank or blank) pathways, AH50 to screen for the (blank) pathway

A

CH50 for the classical or terminal pathways; AH50 for the alternate pathway

79
Q

A low level of both CH50 and AH50 indicates (blank)

A

a deficiency of a complement shared by both pathways, i.e. C3-9

80
Q

low levels of C3 AND C4 suggest activation of which pathway?

A

classical

81
Q

low levels of C3 and NORMAL C4 suggest activation of which pathway?

A

alternate

82
Q

What is the most common complement deficiency?

A

MBL deficiency; can be up to 50% in certain populations

83
Q

MBL deficiency is 2-3x more common in what disorder?

A

SLE

84
Q

How do adults with MBL def. compensate?

A

upregulate production of opsonic Abs

85
Q

A clinical pattern similar to agammaglobulinemia suggest what deficiency?

A

MBL

86
Q

what is the second most common complement deficiency?

A

c2

87
Q

what are the characteristics of C2 def?

A

recurrent MILD infections before 1 year of age

88
Q

What is the molecular defect/result of c2 deficiency?

A

inability for C1q to form C3 convertase after C1q has bound an immune complex

89
Q

Can C3b from lectin and alt. pathways be used in removing immune complexes?

A

NO

90
Q

t/F: there are inherited deficiencies for all complement proteins

A

true

91
Q

What is the molecular cause for inhertied C8 deficiency?

A

mutations in the B chain of C8

92
Q

What infection characterizes a C8 deficiency?

A

RECURRENT NEISSRIA, especially neisseria meningitidis or

93
Q

besides a C8 def, what else does recurrent Neisseeria suggest?

A

defect in the MAC (C5-9), or of factors D and P of the alt. pathway

94
Q

can vaccination overcome complement deficiencies?

A

yes, thorugh production of protective Abs

95
Q

What results in poorly controlled complement system?

A

tissue damage
depletion of critical complements
increased susceptibility to infections and immune complex disease

96
Q

What is the most important complement inhibitor?

A

C1 inhibitor (C1INH)

97
Q

Which complement inhibitor causes paroxysmal nocturnal hemoglobulinemia?

A

CD59 aka protectin

98
Q

What causes hereditary angioedema (HAE)?

A

def. in C1INH

99
Q

C1INH is a (blank) protease inhibitor that prevents C1s and C1r from the (blank) pathway from overactivation

A

serine

classical

100
Q

What vasoactive mediator is overactivated in C1INH def?

A

bradykinin

101
Q

In HAE, bradykinin causes swelling of what?

A

face, intestines, and airways

102
Q

How do you diagnose C1INH def?

A

super low C1INH

NORMAL C3

103
Q

Does HAE respond to epinephrine?

A

NO, that’s how you tell it apart from anaphylaxis!

104
Q

What is the Tx for HAE?

A

human recombinant C1INH

Block 6 Week 1 Colt (11 decks)

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