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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.
The Kell antigen system (also known as the Kell–Cellano system) is a human blood group system, that is, a group of antigens on the human red blood cell surface which are important determinants of blood type and are targets for autoimmune or alloimmune diseases which destroy red blood cells.
One can interpret the CH50 value along with the individual's complement factor values to help determine the etiology. For example, if and individual has normal C3/C4 values but a decreased CH50, that can indicate a terminal complement pathway deficiency while if one has low C3 and CH50 values that can indicate an autoimmune condition such as ...
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.