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Cards In This Set
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Components of membrane attack complex?
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C6-9
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C1q?
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Binds the Fc region of antibody/antigen complexes
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Classical pathway?
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Triggered by antibody bound to antigen, expose binding site for C1q.
C1q has 6 globular heads attached to a central body by collagen-like strands. C1r and C1s proteases bind via C1q and cleave C4 C4b binds via a thioester bond C2 binds C4b and is cleaved to reveal C2a forms the C4b2a convertase. C4b2a recruits and cleaves C3b to form the C3b4b2a convertase |
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C2b?
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Small fragment no known bioactivity
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Lectin pathway?
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MBL is a 6-headed protein similar to C1q which binds mannose.
Bound and stabilised MBL interacts with two serine esterases MASP1 and 2. Activates C4 akin to classical pathway C4b stabilised by formation of C4b2a |
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MASP 1 and 2 analogous to?
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C1r and C1s
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Opsonins C3b and C4b covalent binding?
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- thioester bond protected by C3a
- when cleavage occurs highly unstable reactive intermediate formed. 1/2 life in milliseconds - forms a covalent bond with any surface it is close to - deactivated by cleavage |
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The alternative pathway?
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C3 is a major plasma protein that is spontaneously activated by surface contact
Is constantly being activated in serum but is very short-lived Factor B activation and stabilisation of factor D produces a stable surface C3bBb This accelerates formation of more C3b opsonin to bind at surface |
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Amplification?
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1 C3 convertase can generate 1000 C3b opsonin molecules
Some bacteria also bind a plasma protein that accelerates the alternate pathway by stabilising the C3bBb complex |
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C5 convertase and the effector end of complement?
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The two surface bound complexes C4b2a and C3bBb can cleave both more C3 and also cleave soluble C5 into C5b which initiates the MAC and the smaller fragment C5a. C5a is a potent anaphylatoxin with multiple activities. C3a, C4a and C5a are anaphylatoxins, but C5a is the most potent.
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Why doesn't complement attack normal cells?
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- soluble C4b and C3b are very unstable. Thioester 1/2 life milliseconds. Only active when close to a surface that their activator is bound to.
- A number of soluble factors inhibit complement binding to host cells or accelerate their decay. - Host cells express a number of accessory proteins that destabilise opsonins that might form on them. |
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Serpin?
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C1 inhibitor - binds to activated C1r,s removing it from C1q
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C4BP?
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Binds C4b displacing C2a and destabilising C4b2a
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Factor H?
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Binds C3b displacing Bb. Cofactor for factor I
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Factor I?
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Protease which cleaves C3b and C4b
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