Changes

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

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

*** In plasma or on bacterial surfaces.

*** In plasma or on bacterial surfaces.

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

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

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

*** 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 therefore:

** To coat bacteria with iC3b.

*** A major target for phagocytosis by macrophages and neutrophils via the complement receptors.

** To induce an acute inflammatory response via C3a and C5a.  

*** Chemotactic for neutrophils .

*** Induce the production of the cytokines (IL-1β and TNFα) responsible for acute inflammation.

===CLASSICAL PATHWAY ACTIVATION===

===CLASSICAL PATHWAY ACTIVATION===