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MIMM 214 > Innate Immunity 2 > Flashcards

Innate Immunity 2 Flashcards

1
Q

what is the definition of complement system?

A

group of soluble proteins that work with innate and adaptive immune systems

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2
Q

what are the 3 functions of the complement systems?

A
  1. eliminate pathogens
  2. eliminate dying cells
  3. eliminate immune complexes
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3
Q

what is most of the complement system comprised of?

A

proteases in the blood and other fluids

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4
Q

how many proteases are involved in the complement system?

A

> 30

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5
Q

what is a protease?

A

an enzyme that performs proteolysis

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6
Q

how are proteases in the complement system named? 2 ways

A

have the letter C, followed by a number

some called “factor” followed by a capital letter

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7
Q

how are proteases numbered?

A

based on when they were discovered

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8
Q

where are most complement proteins produced?

A

liver

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9
Q

what are the 3 main mechanisms of action of the complement system?

A
  1. increasing vascular permeability and chemotaxis (inflammation)
  2. destroying pathogen cell membranes so they burst
  3. increasing recognition of pathogens and opsonization
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10
Q

what are the 3 ways that the complement system is activated?

A
  1. classical pathway
  2. alternative pathway
  3. lectin pathway
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11
Q

what are complement proteins called before they are activated?

A

pro-proteases

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12
Q

what 2 fragments are produced by proteolytic cleavage of complement proteins?

A

1 small fragment, 1 large fragment

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13
Q

how is the small fragment named?

A

identified by letter “a” after C#

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14
Q

what type of cleavage is used to cleave complement proteins?

A

proteolytic cleavage

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15
Q

how is the large fragment named?

A

identified by letter “b” after C#

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16
Q

what is the function of the small fragment of cleaved complement protein?

A

has specific function for clearing out the pathogen

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17
Q

what is the function of the large fragment of cleaved complement protein?

A

proteolytic activity on a new substrate

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18
Q

what is C3 convertase?

A

cleaves C3

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19
Q

what are the 2 forms of C3 convertase?

A

C4b2a and C3bBb

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20
Q

where do the pro-proteases (inactive complement proteins) circulate until they become activated?

A

in blood

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21
Q

what is the role of initiators in the complement system?

A

initiate the complement reactions to allow for more complement proteins

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22
Q

what occurs during the complement cascade?

A

cleavage and activation of a complement reaction sequence

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23
Q

what are the 3 main molecules produced from the complement system?

A
  1. opsonins
  2. Anaphylatoxins
  3. membrane attack complex
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24
Q

what does the complement system ultimately trigger?

A

inflammation

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25
Q

what is the role of regulators in the complement system?

A

inhibits formation of MAC on host cells

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26
Q

what are the 4 common things about the 3 complement pathways?

A
  1. all occur on pathogen surfaces
  2. all activate complement
  3. all generate C3 convertase
  4. all promote inflammation, phagocytosis, MAC
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27
Q

what triggers the lectin pathway?

A

lectins

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28
Q

what are lectins?

A

soluble proteins that are PRRs which circulate in blood

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29
Q

what are 2 examples of lectins?

A
  1. mannose-binding lectin (MBL)
  2. ficolins
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30
Q

when does the expression of lectins increase?

A

during infection

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31
Q

where do lectins bind?

A

carbohydrates on the surface of pathogens

32
Q

lectins are an example of _____

A

a PRR

33
Q

what are the 2 main results of the lectin pathway?

A
  1. triggers the signaling cascade on the pathogen surface
  2. generates C4b2a (C3 convertase)
34
Q

what are MASPs and their functions?

A

proteases on the pathogen surface
activated when lectin binds to allow for the cleavage of complementary proteins, cleaves C4 and C2 to make C4b2a

35
Q

what protein binds to the pathogen surface in the classical pathway?

A

C1q

36
Q

is C1q soluble or non-soluble?

A

soluble

37
Q

where does C1q bind? (2)

A
  1. binds pathogens directly
  2. binds antibodies that are bound to pathogen surface
38
Q

when does C1q bind antibodies?

A

when you have previously been infected with an antigen and are now re-infected

39
Q

what complement pathway links the adaptive immunity to innate?

A

classical

40
Q

what are the steps for C3 cleavage in the classical pathway?

A
  1. C1q binds
  2. signaling cascade on pathogen surface is triggered
  3. C4b2a is produced
  4. C3 is cleaved to C3a and C3b
41
Q

which 2 pathways result in activation of C3 convertase (C4b2a)?

A

classical and lectin

42
Q

what is C3a involved in?

A

enhancing inflammation

43
Q

what is C3b involved in? (2)

A
  1. opsonization
  2. C5 convertase (C5a and C5b)
44
Q

when is the alternative pathway activated?

A

once C3b has been produced by the lectin or classical pathway

45
Q

what is the alternative pathway and its purpose?

A

amplifies C3b production and deposits more C3b molecules on the pathogen

46
Q

what does the alternative pathway require? (2)

A
  1. factor B
  2. protease factor D
47
Q

what are the 4 steps of the alternative pathway?

A
  1. C3b deposited on membrane by lectin/classical pathway
  2. C3b binds factor B
  3. factor B is cleaved by plasma protease factor D into Ba and Bb
  4. forms C3bBb complex –> C3 convertase
  5. C3bBb can cleave many more C3 molecules
48
Q

when does C3 undergo spontaneous hydrolysis? and what does it involve?

A

when there is high concentration of C3

involves factors B and protease factor D

49
Q

why is C3bBb different from C4b2a?

A

it is very unstable!! can fall of pathogen surface

50
Q

what stabilizes C3bBb?

A

properdin (factor P)

51
Q

what type of cells secrete properdin/factor P?

A

neutrophils

52
Q

how does properdin/factor P stabilize C3bBb?

A

it binds to some microbial surfaces

53
Q

what do all 3 complement pathways do?

A

activates a C3 convertase to C3a and C3b which has many downstream effects

54
Q

what are 2 results of a complement deficiency?

A
  1. extracellular bacteria are more difficult to clear
  2. complement proteins bind to pathogens in circulation
55
Q

what are 2 complement proteins involved in inflammation?

A
  1. C3a
  2. C5a
56
Q

how do C3a and C5a promote inflammation?

A
  1. recruit phagocytes
  2. increase permeability of blood vessels
57
Q

what causes anaphylactic shock?

A

large amounts of C3a and C5a causing too much fluid leakage from blood vessels

58
Q

what do complement receptors connect?

A

complement receptors connect complement-tagged pathogens to effector cells

59
Q

what do C3a and C5a receptors on granulocytes do?

A

stimulate release of PROINFLAMMATORY CYTOKINES and GRANULE COMPONENTS from basophils, eosinophils, neutrophils, mast cells

60
Q

does the complement system increase or decrease phagocytosis?

A

increase

61
Q

which complement protein do phagocytes have receptors for?

A

C3b

62
Q

how does C3b affect phagocytosis?

A

causes opsonization

63
Q

what are 2 ways that opsonization can occur?

A
  1. complement proteins
  2. antibodies
64
Q

what does MAC stand for?

A

membrane-attack complex

65
Q

what does MAC cause?

A

a pore in the pathogen surface, leading to cell lysis

66
Q

which 2 complement proteins are involved in MAC production

A

C5b and C3b

67
Q

is C5b directly or indirectly involved in MAC?

A

DIRECTLY

68
Q

how is C5b involved in MAC?

A

binds pathogen surface and recruits other complement proteins to form MAC

69
Q

is C3b directly or indirectly involved in MAC?

A

indirectly

70
Q

how is C3b involved in MAC?

A

bc it is a C5 convertase, allowing C5b production which therefore allows MAC production

71
Q

what is the general role of complement-REGULATORY proteins?

A

prevent complement from being activated under normal/basal conditions

72
Q

where are complement-regulatory proteins located?

A

in plasma or cell surfaces

73
Q

how do complement-regulatory proteins prevent complement activation under normal/basal conditions?

A
  1. prevent production C3 convertase
  2. promote destruction of C3 convertase
74
Q

what is an example of a result of complement-regulatory protein activity?

A

inhibited MAC formation by preventing a specific complement protein from binding

75
Q

why are antibodies not considered PRR?

A

bc they are v specific

MIMM 214 (33 decks)

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