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1Principles of Biomedicine - MD1 > 13 - Innate Immunity Components > Flashcards

13 - Innate Immunity Components Flashcards

1
Q 
Ways that commensals protect against infection
1)
2)
3)
4)
A

1) Production of toxic metabolites
2) Production of bacteriocins, antibiotics
3) Competition for binding sites on GIT epithelium
4) Stimulation of antibacterial compound production by epithelial cells through PAMP recognition

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2
Q

MBL (mannan binding lectin) ligand

A

Mannan on bacterial cell wall

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3
Q

Proportion of blood proteins that are complement

A

~10%

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4
Q 
Effects of complement activation
1)
2)
3)
4)
A

1) Inflammation
2) Opsonisation
3) Chemotaxis
4) Lysis of microbes

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5
Q

What are complement proteins?

A

Inactive proteins (often pro-enzymes, zymogens) in serum activated by proteolysis to carry out a range of immune functions

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6
Q

Number of C’ proteins

A

Over 30

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7
Q

What produce C’ proteins?1)2)3)4)

A

1) Hepatocytes
2) Macrophages/monocytes
3) Some epithelial cells
4) Neutrophils (less commonly)

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8
Q

Globin plasma

A

Protein component of plasma

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9
Q

How are C’ activated?

A

Enzymatic cascade

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10
Q

Significance of ‘a’ and ‘b’ fragments of a C’

A

‘a’ is smaller fragment, ‘b’ is larger fragment.Exception is C2, where ‘a’ is larger

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11
Q

Where does activation of C’ often occur?

A

Surface of pathogen

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12
Q

How do host cells minimise self damage by C’?

A

Self cells have regulatory factors on their surfaces for reducing C’ activity.
Pathogens lack these

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13
Q

Activity of soluble/fluid phase C’

A

Often transiently active, inactive.

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14
Q

Which C’ pathway is an effector of humoral immunity?

A

Classical pathway

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15
Q

Alternative pathway origins

A

Evolutionarily older than the lectin or classical pathways

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16
Q

Antibody-independent pathways

A

Lectin, alternative

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17
Q

Steps in C’ cascade1)2)3)

A

1) Initiation
2) Early
3) Late

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18
Q

Initiation 1)2)3)

A

1) 3 pathways for activation
2) Different pathways use different, but homologous components
3) Result in formation of different, but homologous C3 convertases

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19
Q

Early stages1)2)

A

1) Cleavage of C3

2) Formation of C5 convertase

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20
Q

How can C3 be cleaved?1)2)

A

1) C3 convertase (C4b/C2a, C3b/Bb)

2) Spontaneous hydrolysis of C3 (tickover)

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21
Q

Types of C3 convertase1)2)

A

1) Classical/lectin - C4b/C2a

2) Alternative - C3b/Bb

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22
Q

Late steps (effector phase)1)2)

A

1) After C3 cleavage, C5 convertases are formed

2) C5 activation results in pore formation, inflammation, cell lysis

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23
Q

Common steps in complement activation1)2)3)

A

1) C3 convertase cleaves C3 (C4b/C2a or C3b/Bb)
2) C3 is cleaved, C3a is an inflammatory mediator, C3b binds to the surface of microbe (acts as an opsonin)
3) C3 convertases form the C5 convertases (C4b/C2a/C3b or C3b/Bb/C3b)

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24
Q

How does C3b bind to microbial surface?

A

Cleavage exposes reactive thioester groups on C3b

Reactive thioester groups bind amino and hydroxyl groups on microbial surface

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25
Q

Two types of C5 convertase

A

1) Classical/lectin - C4b/C2a/C3b

2) Alternative - C3b/Bb/C3b

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26
Q

Alternative pathway initiation1)2)3)4)5)6)

A

1) Low-levels of C3 hydrolysis initiate formation of active intermediates2) Intermediates cleave C3 to C3a and C3b. In fluid, C3b is short-lived3) C3b thioester group is revealed, C3b binds to microbial surface4) B cleaved by factor D to Bb5) C3b and Bb form C3 convertase on microbial surface6) Properdin binds and stabilises C3 convertase on microbial surface

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27
Q

What cleaves B into Bb?

A

Factor D

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28
Q

What stabilises C3 convertase on microbial surface in alternative pathway?

A

Properdin

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29
Q

How is C5 convertase formed in the alternative pathway?

A

When C3 convertase cleaves C3, C3b joins C3b/Bb on cell surface, forms C5 convertase

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30
Q

Factor Bb1)2)3)

A

1) Active form of factor B
2) Cleaved by factor D
3) Forms alternative C3 convertase with C3b, and alternative C5 convertase with two C3b’s

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31
Q

Factor D1)2)

A

1) Serine protease

2) Cleaves factor B when bound to C3b

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32
Q

How is alternative initial phase regulated?1)2)

A

1) Factors I and H rapidly degrade C3b in fluid phase

2) C3b can bind host-cell surfaces, but is rapidly inactivated by complement regulatory proteins on these cells

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33
Q

Factor I and factor H role

A

Inactivate C3b in fluid phase

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34
Q

What initiates the classical C’ pathway?

A

C1q binding to an antibody or C-reactive protein, bound to a pathogen

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35
Q

C1 structure

A

A compex of C1q (6x collagen-like tails, 6x globular heads), C1r and C1s (serine proteases)

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36
Q

What does C reactive protein bind?

A

Phosphocholine residues on bacterial surfaces

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37
Q

How is C1 activated?

A

C1q binding activates C1r to cleave C1s, which forms an active serine protease

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38
Q

IgGs that best activate classical pathway

A

IgG1, IgG3

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39
Q

Antibody that best activates classical pathway

A

IgM

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40
Q

Minimum number of Ig heavy chains that C1q must bind to activate classical pathway

A

2

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41
Q

Can soluble IgM activate classical pathway?

A

No

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42
Q

How does IgM/IgG activate classical pathway?

A

Binds to pathogen, this results in a conformational change.IgM Fc region involved in C1q binding is exposed

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43
Q

Classical complement pathway formation of C3 convertase1)2)3)4)5)6)7)8)

A

1) C1q binds antibody
2) C1r2, C1s2 are activated
3) C4 binds activated C1q
4) Activated C1s cleaves C4 into C4a, C4b
5) C4b binds covalently to cell surface
6) C4b binds C2
7) C2 is cleaved by C1s8) C4b/C2a C3 convertase formed

44
Q

Classical pathway equivalent to alternative factor B

A

C2

45
Q

Classical pathway equivalent to alternative C3b

A

C4b

46
Q

Classical and alternative formation of C5 convertase1)2)

A

1) C3 convertase cleaves C3 into C3a, C3b

2) C3b binds to C3 convertase, forms C5 convertase

47
Q

C5a

A

Powerful inflammatory mediator

48
Q

C3a

A

Inflammatory mediator

49
Q

Lectin pathway formation of C3 convertase1)2)3)4)5)6)7)

A

1) MBL binds to sugars on microbial surface
2) MBL-associated serine protease (MASP) binds to collagen-like region of MBL
3) MASP cleaves C4 into C4a, C4b (from here on, the same as classical pathway)
4) C4b covalently binds to cell surface
5) C4b binds C2
6) C2 cleaved by MASP into C2a, C2b
7) C4b and C2a form C3 convertase

50
Q

What is MBL equivalent to?

A

C1q

51
Q

Alternative pathway amplification loop1)2)3)4)

A

1) C3b produced by any pathway can interact with factors B and D
2) C3b binds to cell surface with thioester region
3) Factor B is cleaved by factor D
4) Bb binds to C3b, forms C3 convertase

52
Q

Formation of membrane attack complex1)2)3)4)5)6)7)

A

1) C5b bound to cell membrane
2) C5b recruits C6, C7 (hydrophobic)
3) C5b/C6/C7 insert into cell membrane, recruit C8
4) C8 is a trimer. 1 unit inserts into cell
5) C5b/C6/C7/C8 capable of transiently lysing cells
6) C5b/C6/C7/C8 casuses polymerisation of C9
7) Polymerised C9 forms a 100 Angstrom hole

53
Q

Bacteria that is controlled with C9 pore formation

A

Neisseria spp

54
Q

Factors involved in forming classical C3 convertase

A

C1(q, r, s), C2a, C4b

55
Q

Factors involved in forming lectin C3 convertase

A

MBL, MASP, C2a, C4b

56
Q

Factors involved in forming alternative C3 convertase

A

C3b, Bb, factor D (cleaves B)

57
Q

Complement components that act as opsonins

A

C3b, C4b

58
Q

Complement receptors involved in phagocytosis

A

CR1, CR3

59
Q

Another name for CR1

A

CD35

60
Q

Another name for CR3

A

Mac-1CD11bCD18

61
Q

Cells that express CR1 and CR31)2)3)4)

A

1) Macrophages2) Neutrophils3) Follicular dendritic cells4) Erythrocytes

62
Q

What do CR1 and CR3 have a high affinity for?

A

C3b, iC3b, C4b

63
Q

What does CR3 bind?

A

iC3b

64
Q

iC3b

A

Breakdown product of C3b that forms on cell membranes(inactive C3b)

65
Q

What enhances C3b phagocytosis?

A

Specific IgG also binding to microbe

66
Q

Role of CR1 on erythrocytes

A

Binds to C3b/C4b opsonised microbes, transports them to the spleen, where they are destroyedErythrocyte is not destroyed in this process.

67
Q

CR2

1)2)3)4)

A

1) CD21
2) Complement receptor on B cells
3) Complexes with CD19 and CD81
4) Provides a second signal for B cell activation

68
Q

Which cells express CR2?

A

B cellsFollicular dendritic cells

69
Q

What does CR2 bind?

A

iC3b, C3dg antigen/antibody complexes

70
Q

What is C3dg?

A

A C3 breakdown product

71
Q

CR41)2)3)

A

1) Dimer of CD11c and CD182) Present on dendritic cells3) Similar function to CR3

72
Q

Role of complement in B cell activation1)2)3)

A

1) Antigens coated by C3dg bind IgM and CR2
2) Boosts phosphorylation of ITAM residues on Igalpha and Igbeta
3) This amplifies BCR signalling

73
Q

Which complement components are anaphylatoxins?

A

C3a, C5a

74
Q

Effects of C3a and C5a

A

AnaphylatoxinsCause systemic inflammation, which in extreme cases resembles anaphylactic shock

75
Q

Where are C3a and C5a receptors found?1)2)3)

A

1) Mast cells
2) Endothelial cells
3) Phagocytes

76
Q

How do C3a and C5a cause systemic inflammation?1)2)3)

A

1) Bind to mast cells, cause them to release TNFa, histamine
2) Bind to endothelial cells, induce vascular leakage
3) C5a is a chemotactant. Attract neutrophils, monocytes

77
Q

C3aR and C5aR structure

A

Seven-pass transmembrane proteinsGPCR

78
Q

Agents targeted by the complement cascade

A

Extracellular bacteria, free virions, parasites

79
Q

Bacterial factors that activate C’

A

Peptidoglycan and LPS activate the alternative pathway

80
Q

Results of activation of C’1)2)3)4)5)

A

1) Direct lysis2) Inflammation3) Chemotaxis4) B cell activation5) Opsonisation

81
Q

DAF, CR1, MCP roles

A

Regulate C3 convertase productionMembrane-bound

82
Q

Factor I and factor H roles

A

Cleave C3b (to inactivate)

83
Q

CD59 role

A

Inhibit MAC formation

84
Q

Self cells susceptible to C’ lysis

A

ErythrocytesHave low levels of regulatory proteins on surface

85
Q

How can C3 convertase be inhibited?1)2)

A

1) Classical pathway DAF, CR1, MCP bind to C4b, displace C2a from C3 convertase
2) Alternative pathwayDAF, CR1 bind to C3b, displace Bb from C3 convertase complex

86
Q

DAF1)2)3)

A

1) Decay accelerating factor
2) Membrane-bound
3) Bind to C4b or C3b, displace C2a or Bb from C3 convertase

87
Q

MCP1)2)3)4)

A

1) Membrane cofactor protein
2) Membrane-bound
3) Bind to C4b, displace C2a from C3 convertase
4) Can also act as a cofactor for factor I cleaving membrane-bound C3b

88
Q

CR1 roles1)2)3)

A

1) Bind C3b, C4b when these act as opsonins
2) Break down C3 convertase complex by displacing either C2a from C4b, or Bb from C3a
3) Can act as a cofactor for factor I cleaving membrane-bound C3b

89
Q

Factor I1)2)3) a,b

A

1) Serine protease
2) Inactivates fluid-phase C3b
3) Requires additional cofactors to cleave cell-membrane-bound C3ba) Factor H b) MCP or CR1

90
Q

Factor H1)2)

A

1) Cofactor for factor I cleavage of cell-membrane-bound C3b2) Binds to sialic acid, which is highly expressed on mammalian cells.

91
Q

Products of factor I cleavage of C3b

A

iC3b, C3d, C3dg (which bind CR on B cells and phagocytes)

92
Q

CD591)2)

A

1) Cell-membrane-bound protein

2) Binds to C5a on C5b/C6/C7/C8 complex, inhibits C9 from forming pore

93
Q

Effect of C’ on immune complexes

A

Promotes solubilisation of antibody-antigen complexes

94
Q

What determines the ABO blood groups?

A

Allelic difference in enzymes that modify glycans on cell surfaces

95
Q

A allele in blood groups

A

Encodes enzyme that transfers an N-terminal acetylgalatosamine onto glycans

96
Q

B allele in blood groups

A

Encodes an enzyme that transfers a terminal galactose residue onto glycans

97
Q

O allele in blood groups

A

Doesn’t encode an enzyme to modify cell-surface glycans

98
Q

Immune component enforcing blood groups

A

Natural IgM produced against missing allele

99
Q

Classical pathway deficiencies

A

Missing C1, C2, C4

Leads to immune complex disease (EG: systemic lupus erythematosus)

100
Q

Alternative pathway deficiencies

A

Missing B, D, properdinIncreased risk of disease from Neisseria gonorrhoeae or meningitidis

101
Q

Alternative and classical pathway deficiencies

A

Deficiencies in C3 or factors I or HIncreased infections with Strep pneumoniae, Neisseria spp, Haemophilus influenzae

102
Q

What do deficiencies in factors I and H do?

A

Mimic C3 deficiencies

103
Q

How can microbes evade C’?1)2)3)

A

1) Recruit host C’ regulatory proteins
2) Mimic human C’ proteins
3) Inhibit C’-mediated inflammation

104
Q

How do microbes recruit host C’ regulatory proteins?1)2)3)

A

1) Express or scavenge sialic acid (this recruits factor H)2) Synthesise or recruit factor H (EG: gp41 of HIV)3) Viruses incorporate host regulatory proteins into envelope when budding (EG: HIV recruits DAF, CD59)

105
Q

Microbe that mimics human C’ proteins

A

E coli has a C1q binding protein

106
Q

Microbe that inhibits C’-mediated inflammation

A

Staph aureus, using CHIPS (chemotaxis inhibitory protein of Staph aureus)

107
Q

When do C’ deficiencies normally present?

A

~6-9 months after birth

1Principles of Biomedicine - MD1 (157 decks)

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