Changes

** C3bB¯b3b is one of the two enzymes that activates the Membrane Attack Complex (MAC).

** C3bB¯b3b is one of the two enzymes that activates the Membrane Attack Complex (MAC).

*** Splits C5 into C5a (a small peptide) and C5b (the initiator of the MAC).  

*** Splits C5 into C5a (a small peptide) and C5b (the initiator of the MAC).  

At the same time the complement inhibitors Factors I and H are acting to breakdown C3b to iC3b (whether as single C3b or in the complex (C ) in plasma or on bacterial surfaces; although iC3b is inactive in participating in the complement cascade it is the major target for phagocytes – as these cells have large numbers of cellular receptors for iC3b (complement receptors) that they use to promote phagocytosis (opsonization).  

* At the same time as C3bB¯b3b is being formed, Factors I and H are acting to breakdown C3b to iC3b.

*** As single C3b or in the complex C3b¯Bb.

*** In plasma or on bacterial surfaces.

** iC3b is inactive in the complement cascade it is a major target for phagocytes.

*** Phagocytes have large numbers of iC3b receptors (complement receptors) which give opsonization when engaged.  

The main effects of alternative complement activation are; (1) to coat bacteria with iC3b which is a major target for phagocytosis by macrophages and neutrophils via the complement receptors, and (2) to induce an acute inflammatory response via C3a and C5a. These ‘anaphylatoxins’ are chemotactic for neutrophils and induce the production of the cytokines that are responsible for acute inflammatory (IL-1β and TNFα).

The main effects of alternative complement activation are; (1) to coat bacteria with iC3b which is a major target for phagocytosis by macrophages and neutrophils via the complement receptors, and (2) to induce an acute inflammatory response via C3a and C5a. These ‘anaphylatoxins’ are chemotactic for neutrophils and induce the production of the cytokines that are responsible for acute inflammatory (IL-1β and TNFα).