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This rare condition mutates or prevents C3 protein from forming, lowering the immune system's ability to protect. [17] C4: C4 deficiency is highly associated with systemic lupus erythematosus. [3] Aβ42, a protein involved in Alzheimer's disease, can cause activation of C4 (even in plasma deficient of C1q). [18]
Complement component 3 (C3) is a protein involved in both the innate and adaptive immune response. C3 is one of over 30 complement proteins circulating in the blood. [3] C3 circulates in an inactive form but can be activated in order to aid the immune system's response to a foreign invader. [4]
In contrast, any individual with increased complement levels or activity would have an elevated CH50 since increasing dilution would be necessary to reach the 50% lyse marking. Decreased CH50 values may be seen in cirrhosis or hepatitis [ 6 ] as a result of impaired complement production in the liver.
Leukopenia, thrombocytopenia, Coombs' test, complement activation: low serum concentrations of C3 and C4, positive immunofluorescence using Crithidia luciliae as substrate, antiphospholipid antibodies (i.e. anticardiolipin, lupus anticoagulant, false-positive VDRL) Goodpasture's disease: Anti-glomerular basement membrane antibody
Levels of C3 in the blood may be measured to support or refute a particular medical diagnosis. For example, low C3 levels are associated with Systemic Lupus Erythematosus (SLE) [17] and some types of kidney disease such as post-infectious glomerulonephritis, membranoproliferative glomerulonephritis, and shunt nephritis.
In particular, the use of ELISA proves to be one of the most effective methods of detecting properdin deficiency, as the average healthy male is expected to show properdin antigen levels of around 128.0 ELISA units/ml, and obligate carrier females (recall that properdin deficiency is an X-linked disease) tend to show an average of 45.6 units/ml ...
The result is a leukocytoclastic vasculitis. [2] This results in hypocomplementemia, a low C3 level in serum. [2] They can also cause more reactions, causing the typical symptoms of serum sickness. This is similar to a generalised Arthus reaction. [2]
C2b diffuses into the plasma as a protein inflammatory mediator while C2a remains attached with C4b, forming the C3-convertase (C4b2a). The function of the membrane-bound C3-convertase is the cleavage of many many molecules of C3 into C3a and C3b. C3a is a smaller fragment of C3 is a potent inflammatory mediator.