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BACTERIAL COMPLEMENT ESCAPE

Pathogen-Derived Immunomodulatory Molecules, edited by Padraic G. Fallon. [Pg.32]

Ihe AP is either activated by spontaneous hydrolysis of the internal thioester bond in C3 (formii C3(H20)) or by covalent attachment of C3b to bacterial surfaces via the CP and LP. Kun or B binds to both surface-bound C3b and fluid-phase C3(H20) and is in turn cleaved by factor D to form a fluid-phase C3 convertase C3(H20)Bb or a surfoce-bound C3bBb complex.  [Pg.33]

The AP C3 convcrtase is positively regulated by properdin, a multimeric protein that increases the stability of the complex.  [Pg.34]

Complement was first identified as a heat-labile principle in serum that complemented antibodies in the killing of bacteria. Now is known that complement is a system of more than 30 proteins in plasma and on cell surfaces that interact with each other in an orderly hion that is referred to as the complement cascade . Complement and complement evasion by bacteria is addressed in a different chapter ( Bacterial complement escape by Jongerius, Ram and Rooijakkers) and in recent reviews. ... [Pg.21]

See other pages where BACTERIAL COMPLEMENT ESCAPE is mentioned: [Pg.32]    [Pg.33]    [Pg.35]    [Pg.37]    [Pg.39]    [Pg.43]    [Pg.45]    [Pg.47]    [Pg.32]    [Pg.33]    [Pg.35]    [Pg.37]    [Pg.39]    [Pg.43]    [Pg.45]    [Pg.47]    [Pg.276]    [Pg.346]    [Pg.162]   


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