BIOL 2050U Lecture Notes - Chemotaxis, Vitronectin, Complement Factor B

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30 Jan 2013
Outline of Lecture 07
I. Overall principles of complement
1) Two overall phases: enzymatic and lytic (pore forming)
2) Split products are formed during complement cascade, both products are
biologically active
3) There are three ways to activate C’, and all converge at C3
II. There are three ways to activate C’
1) Classical Pathway
Activated by C1 binding to IgM or IgG which are bound to Ag
Specifically, C1q portion binds two Fc regions, then C1r/C1s cleaves C4
C4b reacts fast, e.g. covalently binds bacterial cell surface whereas C4a
remains soluble
C4b binds C2, C1s cleaves C2, results in C4b2a complex (the C3
2) Mannose Binding Lectin
MBL is homologous to C1, but does not require antibody to activate
Like C1, MBL cleaves C2 and C4 to create the C3 convertase
3) Alternative Pathway
C3 can “tickover”, i.e. spontaneously covalently bind surfaces
In appropriate environment, C3 complexes with B; B is cleaved by D
C3bBb complex recruits properdin (P); this is a C3 convertase
III. Further down the complement cascade
A) What C3 does
C3a is anaphylactic: causes mast cells and basophils to release histamine
C3b collects around the C3 convertase (ground zero) and opsonizes target
(phagocytes have complement receptor, CR1)
Phagocytosis greatly enhanced by C3 and bound Ab
C3b when bound to either C3 convertase becomes a C5 convertase
B) What C5 does
C5a is anaphylactic and a chemoattractant for granulocytes
C5b recruits C6 and C7, which inserts into target cell membrane
C8 and lots of C9 join, forming membrane attack complex (MAC)
MAC is a membrane pore, causes lysis of target cell
IV. Regulation
A) C1
- C1-inhibitor is a suicide substrate for C1
B) Classical C3 convertase
- DAF and CR1 promote dissociation of C4b2a
- Factor I inactivates C4b by cleavage
C) Alternative C3 convertase
- Factor H binds C3b instead of factor B on cells with sialic acid
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