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Infection and immunity 2 > Complement 2 > Flashcards

Complement 2 Flashcards

1
Q

what are the 2 additional roles of complement?

A

phagocytosis

clearance

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2
Q

how is complement involved in phagocytosis?

A
  1. antibodies bound to bacteria activate complement and bonding of C3b to bacteria
  2. engulfment of bacteria by neutrophils is mediated by Fc receptors + complement receptors
  3. granules fuse with phagosomes, releasing toxic oxygen metabolites that kill bacteria
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3
Q

how is complement involved in clearance?

A
  1. small antigen-antibody complexes form and activate complement
  2. complex gated with C3b
  3. bound C3b binds to Cr1 on erythrocyte surface
  4. delivers immune complexes to spleen + liver, where they are removed
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4
Q

what are the 4 main complement receptors and their ligands?

where are these found?

A

CR1

  • CD35
  • erythrocytes

CR2

  • CD21
  • B and T cells

CR3

  • CD11b+CD18
  • neutrophils

CR4

  • CD11c+CD18
  • neutrophils
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5
Q

what do the 4 main complement receptors have in common?

A

complement control repeat protein receptors

beta-2 intern family adhesion molecules

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6
Q

what are the 2 anaphylatoxin receptors?

where are they expressed?

what type of receptors are these?

A

C3a receptor
- widely expressed

C5a receptor
- lymphoid cells

GPCR

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7
Q

which molecules are important for regulating complement activation?

A

DAF
= decay accelerating factor

factor I
= C3b/C4b inactivator

factor H
= co=factor for factor I

MCP
= membrane cofactor protein

CR1
= complement receptor 1

C4BP
= C4 binding protein

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8
Q

what do CR1 and DAF do?

A

compete with Factor B in binding with C3b on the cell surface

they can even remove Bb from an already formed C3bBb complex

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9
Q

what does factor I do?

which other molecules does it require?

A

cleaves C3b into its inactive form iC3b
-> brevets C3 convertase formation

requires a C3b-binding protein like factor H, CR1 + MCP

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10
Q

what does factor H do?

what does it preferentially bind too and what does this result in?

A

inhibits formation of C3 convertase by competing with factor B for binding to C3b

accelerates the decay of C3 convertase

acts as a cofactor for factor I-mediated cleavage of C3b

vertebrate cells (high affinity for GAGs)
-> protects host cells from complement-mediate damage
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11
Q

describe the structure of factor H

what do these domains bind to?

A

4 complement control repeat units at the N terminus
- binds to C3b on surface of cells

2 domains (19 +20)

  • bind to C3b
  • bind to sugars on host cells
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12
Q

how does factor H react differently to self and non-self cells?

A

non-self
= weak binding
-> activation

self
= strong binding to GAGs and C3b
-> regulation

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13
Q

what have some microbes now developed?

A

immune evasion proteins that help factor H bind

-> breakdown of C3b

= evade complement activation on their surfaces

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14
Q

what are these immune evasion proteins/mechanisms that microbes have evolved?

A

C3 convertase inhibitors

protease production
-> breakdown +ve complement fragments of microbial surface

RCA-like expression

binding of RCA
(complement regulators)

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15
Q

explain how C4bp and factor H promote the dissociation of C3 convertases

what else are these molecules involved in?

A

C4bp acts on C4b2b
factor H acts on C3bBb

they bind to the covalently bound component (C4b or C3b)
-> displaces the associated cofactor

C4bp, fH, CR1 + MCP
catalyse the permanent inactivation of C3b and C4b via proteolytic cleavage by factor I

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16
Q

what do complement deficiencies result in?

A

increased susceptibility to bacterial infections e.g. meningococcal disease

autoimmune diseases

17
Q

what is the name of the disease caused by a C4 deficiency?

A

systemic lupus erythematosus (SLE)

18
Q

what are the features of C2 deficiency?

A

most common of the inherited classical complement component deficiencies in Caucasians

most common cause of death = sepsis

most common organisms: S. pneumoniae and H. influenzae

19
Q

what are the features of C3 deficiency?

A

rarest fo the 4 early component deficiencies

most severe phenotype

Membranoproliferative glomerulonephritis

neutrophil dysfunction
humoral deficiencies
complement deficiencies

20
Q

what are the features of factor B deficiency?

A

single case has been reported

meningococcemia

21
Q

what are the features of factor D deficiency?

A

Neisserial infections are the most common manifestation

22
Q

what are the features properdin deficiency?

A

X-linked complement deficiency

1 of more common complement deficiencies + occurs largely in Caucasians

1 or more episodes of meningococcal disease

high fatality rate

Infection and immunity 2 (13 decks)

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