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Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. Complement factor I (factor I) is a protein of the complement system , first isolated in 1966 in guinea pig serum , [ 5 ] that regulates complement activation by cleaving cell-bound or fluid phase C3b and C4b. [ 6 ]
Mothers who are negative for the Kell 1 antigen develop antibodies after being exposed to red blood cells that are positive for Kell 1.Over half of the cases of hemolytic disease of the newborn owing the anti-Kell antibodies are caused by multiple blood transfusions, with the remainder due to a previous pregnancy with a Kell 1 positive baby.
Atypical hemolytic uremic syndrome (aHUS), also known as complement-mediated hemolytic uremic syndrome (not to be confused with hemolytic–uremic syndrome), is an extremely rare, life-threatening, progressive disease that frequently has a genetic component. In most cases, it can be effectively controlled by interruption of the complement cascade.
Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis, [1] [2] is an alloimmune condition that develops in a fetus at or around birth, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta.
First, the proteolytic component of the convertase, Bb, is removed by complement regulatory proteins having decay-accelerating factor (DAF) activity. Next, C3b is broken down progressively to first iC3b, then C3c + C3dg, and then finally C3d. Factor I is the protease cleaves C3b but requires a cofactor (e.g Factor H, CR1, MCP or C4BP) for activity.
Blood compatibility testing is routinely performed before a blood transfusion.The full compatibility testing process involves ABO and RhD (Rh factor) typing; screening for antibodies against other blood group systems; and crossmatching, which involves testing the recipient's blood plasma against the donor's red blood cells as a final check for incompatibility.
Factor I requires a C3b-binding protein cofactor such as complement factor H, CR1, or membrane cofactor of proteolysis (MCP or CD46) Complement factor H can inhibit the formation of the C3 convertase by competing with factor B for binding to C3b; [ 1 ] accelerate the decay of the C3 convertase; [ 2 ] and act as a cofactor for factor I-mediated ...
Activation of the C1 complex initiates the classical complement pathway. This occurs when C1q binds to antigen-antibody complexes. The antibodies IgM or certain subclasses of IgG complexed with antigens are able to initiate the complement system: a single pentameric IgM can initiate the pathway, while several monomeric IgG molecules are needed. [3]