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Immunology > Lecture 26 - Complement Proteins II > Flashcards

Lecture 26 - Complement Proteins II Flashcards

1
Q

Complement components that act as opsonins

A

C3b, C4b

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2
Q

Complement receptors involved in phagocytosis

A

CR1, CR3

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3
Q

Another name for CR1

A

CD35

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4
Q

Another name for CR3

A

Mac-1

CD11bCD18

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5
Q 
Cells that express CR1 and CR3
1)
2)
3)
4)
A

1) Macrophages
2) Neutrophils
3) Follicular dendritic cells
4) Erythrocytes

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6
Q

What do CR1 and CR3 have a high affinity for?

A

C3b, iC3b, C4b

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7
Q

What does CR3 bind?

A

iC3b

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8
Q

iC3b

A

Breakdown product of C3b that forms on cell membranes

inactive C3b

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9
Q

What enhances C3b phagocytosis?

A

Specific IgG also binding to microbe

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10
Q

Role of CR1 on erythrocytes

A

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

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11
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

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12
Q

Which cells express CR2?

A

B cells

Follicular dendritic cells

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13
Q

What does CR2 bind?

A

iC3b, C3dg antigen/antibody complexes

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14
Q

What is C3dg?

A

A C3 breakdown product

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15
Q

CR4
1)
2)
3)

A

1) Dimer of CD11c and CD18
2) Present on dendritic cells
3) Similar function to CR3

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16
Q

Role of complement in B cell activation
1)
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

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17
Q

Which complement components are anaphylatoxins?

A

C3a, C5a

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18
Q

Effects of C3a and C5a

A

Anaphylatoxins

Cause systemic inflammation, which in extreme cases resembles anaphylactic shock

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19
Q

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

A

1) Mast cells
2) Endothelial cells
3) Phagocytes

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20
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

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21
Q

C3aR and C5aR structure

A

Seven-pass transmembrane proteins

GPCR

22
Q

Agents targeted by the complement cascade

A

Extracellular bacteria, free virions, parasites

23
Q

Bacterial factors that activate C’

A

Peptidoglycan and LPS activate the alternative pathway

24
Q 
Results of activation of C'
1)
2)
3)
4)
5)
A

1) Direct lysis
2) Inflammation
3) Chemotaxis
4) B cell activation
5) Opsonisation

25
Q

DAF, CR1, MCP roles

A

Regulate C3 convertase production

Membrane-bound

26
Q

Factor I and factor H roles

A

Cleave C3b (to inactivate)

27
Q

CD59 role

A

Inhibit MAC formation

28
Q

Self cells susceptible to C’ lysis

A

Erythrocytes

Have low levels of regulatory proteins on surface

29
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 pathway
DAF, CR1 bind to C3b, displace Bb from C3 convertase complex

30
Q

DAF
1)
2)
3)

A

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

31
Q 
MCP
1)
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

32
Q

CR1 roles
1)
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

33
Q

Factor I
1)
2)
3) a,b

A

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

34
Q

Factor H
1)
2)

A

1) Cofactor for factor I cleavage of cell-membrane-bound C3b

2) Binds to sialic acid, which is highly expressed on mammalian cells.

35
Q

Products of factor I cleavage of C3b

A

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

36
Q

CD59
1)
2)

A

1) Cell-membrane-bound protein

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

37
Q

Effect of C’ on immune complexes

A

Promotes solubilisation of antibody-antigen complexes

38
Q

What determines the ABO blood groups?

A

Allelic difference in enzymes that modify glycans on cell surfaces

39
Q

A allele in blood groups

A

Encodes enzyme that transfers an N-terminal acetylgalatosamine onto glycans

40
Q

B allele in blood groups

A

Encodes an enzyme that transfers a terminal galactose residue onto glycans

41
Q

O allele in blood groups

A

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

42
Q

Immune component enforcing blood groups

A

Natural IgM produced against missing allele

43
Q

Classical pathway deficiencies

A

Missing C1, C2, C4

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

44
Q

Alternative pathway deficiencies

A

Missing B, D, properdin

Increased risk of disease from Neisseria gonorrhoeae or meningitidis

45
Q

Alternative and classical pathway deficiencies

A

Deficiencies in C3 or factors I or H

Increased infections with Strep pneumoniae, Neisseria spp, Haemophilus influenzae

46
Q

What do deficiencies in factors I and H do?

A

Mimic C3 deficiencies

47
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

48
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)

49
Q

Microbe that mimics human C’ proteins

A

E coli has a C1q binding protein

50
Q

Microbe that inhibits C’-mediated inflammation

A

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

51
Q

When do C’ deficiencies normally present?

A

~6-9 months after birth

Immunology (30 decks)

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