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IHL > Complement > Flashcards

Complement Flashcards

1
Q

fxns of C’

A

triggering and amplification of inflammation rxns
chemotaxis for phagocytes
clearance of immune complexes
direct microbial killing

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2
Q

classical C5 convertase

A

C4b2a3b

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3
Q

alternative C5 convertase

A

C3bBb3b

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4
Q

activation of classical C’ pathway

A

Ab binding Ag

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5
Q

activation of alternative C’ pathway

A

independent of Ab

constant “trickle” of activated C’ for surveillance

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6
Q

activation of lectin C’ pathway

A

binding of a serum mannose binding protein to bacteria

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7
Q

diagram classical C’ pathway

A

1) C1q/2C1r/2C1s (C1) binds to multiple Fc of immune complex -> C1qrs
2) C1qrs + C4 -> C4b + C4a
3) C4b clusters near bound Ab, attracts C2
4) C1qrs + C2 -> C2a + C2b
5) C2a associates w/ C4b -> C4b2a (C3 convertase)
6) C3 convertase + C3 -> C3a + C3b
7) C3b deposits on non-self surfaces or associates w/ C4b2a -> C4b2a3b (C5 convertase)
8) C5 convertase + C5 -> C5a + C5b
9) C5b + C6 + C7 -> C5b67
10) C5b67 inserts into membrane, forms small pore -> slow lysis of target cell
11) C8 associates w/ C5b67, recruits 10-16 C9
12) C9 polymerizes, forms large pore in membrane -> osmotic lysis

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8
Q

diagram alternative C’ pathway

A

1) C3 -> C3a + C3bi (spontaneous!)
2) C3bi binds to membranes w/ low levels of sialic acid
3) Factor B binds C3bi
4) Factor D + Factor B -> Ba + Bb
5) C3bi + Bb -> C3bBb (C3 convertase)
6) properdin (P) + C3bBb -> C3bBbP (increases half-life of C3 convertase)
7) C3bBbP + C3b -> C3bBb3bP (C5 convertase)
8) C5 convertase + C5 -> C5a + C5b
9) C5b + C6 + C7 -> C5b67
10) C5b67 inserts into membrane, forms small pore -> slow lysis of target cell
11) C8 associates w/ C5b67, recruits 10-16 C9
12) C9 polymerizes, forms large pore in membrane -> osmotic lysis

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9
Q

diagram lectin C’ pathway

A

1) mannose binding lectin (MBL) or ficolin binds mannose
2) MBL/ficolin bind MBL-associated serine proteases (MASPs); structurally similar to C1 complex
3) MBL/MASP + C4 + C2 -> C4a + C4b + C2a + C2b
4) C4b clusters near bound Ab, attracts C2a
5) C2a associates w/ C4b -> C4b2a (C3 convertase)
6) C3 convertase + C3 -> C3a + C3b
7) C3b deposits on non-self surfaces or associates w/ C4b2a -> C4b2a3b (C5 convertase)
8) C5 convertase + C5 -> C5a + C5b
9) C5b + C6 + C7 -> C5b67
10) C5b67 inserts into membrane, forms small pore -> slow lysis of target cell
11) C8 associates w/ C5b67, recruits 10-16 C9
12) C9 polymerizes, forms large pore in membrane -> osmotic lysis

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10
Q

C’ regulation - component half-life

A

many C’ components undergo spontaneous inactivation as they diffuse away from the site of activation

C4b/C3b hydrolyze rapidly -> limits C4b/C3b deposition to nearby cells, limits formation of C3/C5 convertases

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11
Q

C’ regulation - C1inh (C1 inhibitor) - MOA

A

binds to C1r, C1s and MASP molecules

dissociates them from C1q/MBL complex

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12
Q

C’ regulation - Factor I - MOA

A

also C3b inactivator

cleaves C4b or C3b, prevents formation of C3/C5 convertases

requires co-factors

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13
Q

C’ regulation - C4-bp - MOA

A

binds C4b, prevents association w/ C2a

causes C4b to dissociate from C3 convertase

C4b/C4-bp targeted for digestion by Factor I

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14
Q

C’ regulation - complement receptor 1 (CR1) - MOA

A

also CD35

binds C3b molecules, allows cleavage by Factor I

mechanism for distinguishing btw self and non-self

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15
Q

C’ regulation - membrane co-factor protein (MCP) - MOA

A

also CD46

co-factor for Factor I

binds C4b/C3b

MCP is found on self membranes, helps distinguish btw self and non-self

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16
Q

C’ regulation - Factor H - MOA

A

analogous to C4-bp but binds C3b

prevents formation of C5 convertase

Factor H/C3b complex targeted by Factor I

17
Q

describe the protected site concept

A

Factor H binding only occurs if C3b has been deposited on surface of self cell

deposition of C3b on microorganism means it is “protected” from Factor H -> activation of alternative C’ pathway

18
Q

C’ regulation - decay-accelerating factor (DAF) - MOA

A

also CD55

promotes dissociation of C3 convertase (C2a from C4b, Bb from C3b)

19
Q

C’ regulation - CD59 - MOA

A

blocks C9 binding to C5b678 complex

20
Q

C’ regulation - vitronectin (S protein) - MOA

A

binds to fluid phase C5b67, prevents binding to membranes

does NOT prevent association w/ C8 and C9

MAC has no effect since it is not within a membrane

21
Q

major opsonins of opsonization

A

C3b: due to abundance

C4b

C5a (anaphylatoxin): increases expression of C’Rs on surface of phagocytes

22
Q

how are immune complexes removed from circulation?

A

1) IC opsonized w/ C3b/C4b
2) IC binds CR1 on RBC
3) IC transported to hepatic macrophage, becomes bound to it
4) IC/RBC bond broken -> RBC returns to circulation
5) liver metabolizes IC

23
Q

how are self cells protected from MAC?

A

nucleated cells are more resistant to C’-mediated lysis

require formation of multiple MACs to destroy cell

many nucleated cells can endocytose MAC (including cancer cells)

single MAC can lyse RBC (anucleate)

24
Q

anaphylatoxins - fxns

A

C5a is most potent mediator

bind to receptors on mast cells and basophils -> induce degranulation

induce smooth muscle contraction -> increased vascular permeability

induce monocytes and neutrophils to adhere to vascular endothelium -> increased extravasation

25
Q

produces edema through cleavage to kinin by plasmin

A

C2b (prokinin)

26
Q

C3 deficiency - effects; similar conditions?

A

life-threatening

severe, recurrent infxns soon after birth

Factor H/I deficiencies mimic -> unregulated C3b generation by C3 convertase completely exhausts C3 from serum

27
Q

MAC deficiencies (C5-C9) - effects

A

generally healthy individuals

increased infxn w/ *Neisseria gonorrhoeae *and Neisseria meningitidis

28
Q

C2 deficiency - effects

A

most commonly identified form of C’ deficiency

high degree of systemic lupus erythematosis (SLE) -> may arise from failure to efficiently clear circulating ICs

IC deposition on endothelium -> activation of C’ -> inflammation -> possible breakdown of tolerance to self Ags -> autoimmunity

29
Q

C1inh deficiency - effects

A

C4 and C2 levels chronically low

hereditary angioneurotic edema (HANE): swelling attacks w/ no obvious cause; commonly involves extremities, face and GI tract; tx w/ androgens has produced near-normal levesl of C1inh in some pts

30
Q

DAF deficiency - effects

A

paroxysmal nocturnal hemoglobinuria (PNH) (most pts wake up in the morning and urinate blood)

spontaneous episodes of hemolysis

RBCs, WBCs and platelets have increased sensitivity to C’ lysis

tx: EPO

31
Q

viruses that use C’ components to increase infectivity

A

Epstein-Barr: uses CR2 as receptor for attachment

measles: uses MCP (CD46) as receptor for attachment

West Nile: C3b coats viral particle, enters cells via CR3 receptor

IHL (12 decks)

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