Changes

*** Exerts control on the classical pathway.  

*** Exerts control on the classical pathway.  

* '''Factors I and H'''

* '''Factors I and H'''

** function to breakdown C3b hence controlling positive feedback by inhibiting C and preventing the complement cascade from running to exhaustion each time it is activated. Complement receptor 1 (CR1) is present on many cell types especially RBCs; it functions to bind C3d - the breakdown product of C3b – resulting from the action of Factors I and H. On it binds potentially inflammatory immune complexes in plasma; these are then transported to the liver where they are phagocytosed by the hepatic macrophages and removed. A common inflammatory disease resulting from poorly eliminated immune complexes is globerulonephritis. Finally there is the other membrane-associated inhibitor - CD59. This binds the first molecule of C9 when it inserts into a cell membrane. This prevents the polymerisation of C9 obviating pore formation and cell lysis. It acts as a protective mechanism for the host cells.

** Break down C3b.

*** Controls positive feedback by inhibiting C3b¯Bb.

**** Prevents the complement cascade from running to exhaustion each time it is activated.

* '''Complement receptor 1''' ('''CR1''') is present on many cell types especially RBCs; it functions to bind C3d - the breakdown product of C3b – resulting from the action of Factors I and H. On it binds potentially inflammatory immune complexes in plasma; these are then transported to the liver where they are phagocytosed by the hepatic macrophages and removed. A common inflammatory disease resulting from poorly eliminated immune complexes is globerulonephritis.  

Finally there is the other membrane-associated inhibitor - CD59. This binds the first molecule of C9 when it inserts into a cell membrane. This prevents the polymerisation of C9 obviating pore formation and cell lysis. It acts as a protective mechanism for the host cells.

==COMPLEMENT ASSOCIATED DISEASES==

==COMPLEMENT ASSOCIATED DISEASES==