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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 ]
Complement deficiency is an immunodeficiency of absent or suboptimal functioning of one of the complement system proteins. [4] Because of redundancies in the immune system, many complement disorders are never diagnosed. Some studies estimate that less than 10% are identified. [5]
The complement fixation test is an immunological medical test that can be used to detect the presence of either specific antibody or specific antigen in a patient's serum, based on whether complement fixation occurs. It was widely used to diagnose infections, particularly with microbes that are not easily detected by culture methods, and in ...
The complement system, also known as complement cascade, is a part of the humoral, innate immune system and enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. [1]
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.
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.
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 ...
Complement is responsible for immune inflammatory response in adipose tissues which has been implicated in the development of obesity. [8] Obesity in turn results in an abnormally high level of complement activation via production of the C1 component of the classical pathway, which can lead to tissue inflammation and eventually insulin ...