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Complement Associated Diseases (view source)
Revision as of 10:11, 6 September 2007
, 10:11, 6 September 2007→Alternative Pathway Activation
* C3b¯Bb can also bind C3b to form C3bB¯b3b.
* C3b¯Bb can also bind C3b to form C3bB¯b3b.
** 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).
*** C3bB¯b3b splits C5 into:
**** C5a, a small pro-inflammatory peptide.
**** C5b, the initiator of the MAC.
* At the same time as C3bB¯b3b is being formed, Factors I and H are acting to breakdown C3b to iC3b.
* At the same time as C3bB¯b3b is being formed, Factors I and H are acting to breakdown C3b to iC3b.
** The C3b being broken down may be:
** The C3b being broken down may be:
** iC3b is inactive in the complement cascade but 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 therefore:
* The main effects of alternative complement activation are therefore:
** To coat bacteria with iC3b.
** To coat bacteria with iC3b.
*** A major target for phagocytosis by macrophages and neutrophils via the complement receptors.
*** A major target for phagocytosis by macrophages and neutrophils via the complement receptors.