Changes

* Complement is a very powerful system that can be triggered by only small stimuli.

* Complement is a very powerful system that can be triggered by only small stimuli.

** Inappropriate activation can therefore be harmful.  

** Inappropriate activation can therefore be harmful.  

* Complement activation must therefore be tightly controlled.  

* Complement activation must therefore be tightly controlled.

Consequently a range of control mechanisms has evolved to control this. Decay accelerating factor (DAF) is present on cell membranes as well as a secreted product; it hastens the degradation of C1 esterase and controls the Classical Pathway. 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.

** There is a range of control mechanisms.

* ''' Decay accelerating factor''' ('''DAF''')

** Is both secreted and present on cell membranes.

** Hastens the degradation of C1 esterase.

*** Exerts control on the classical pathway.  

* '''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.

==COMPLEMENT ASSOCIATED DISEASES==

==COMPLEMENT ASSOCIATED DISEASES==