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I am thinking the pathogenesis of the C5a in GBS. I think the pathogenesis happens like

C5a-peptidase in acid environment (Sialic acid, capsule) $\to$ cleaves C'-derived Neu chemoattractant C5a $\to \downarrow$ alternative pathway of Complement.

However, this part cleaves C'-derived Neu chemoattractant C5a is not clear to me. I think this means that C5a-peptidase cleaves Neu C5a from the previous complement reaction that inhibits the next coming alternative pathway of complement.

How does this pathogenesis of GBS happen?

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I think "neu" must be an abbreviation for "neutrophil".

C3a and C5a are both chemotactic peptides that recruit cells to sites where complement activation is occurring. C5 is a substrate for the C5 convertases formed in one of the three complement pathways (classical, lectin, alternative). C5b, the other product of this cleavage goes on to form the membrane attack complex.

C5a peptidase is a Streptococcal product which destroys the C5a peptide before it can recruit neutrophils and other agents of cell-mediated immunity. Streptococci also produce an inhibitor of the membrane attack complex.

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