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The complement system is a major component of innate and adaptive immunity; upon activation, the complement results in the formation of the membrane attack complex (MAC) which releases peptides called anaphylatoxins. About 90% of complement components are synthesized in the liver and are acute-phase proteins. C3 activation involves cleavage by C3 convertase into C3a and C3b. Severe recurrent bacterial infections occur in patients with homozygous C3 deficiency and in those patients with low levels of C3, secondary to the absence of C3b activator. Decreased C3 may be associated with acute glomerulonephritis, membranoproliferative glomerulonephritis, immune complex disease, active systemic lupus erythematosus, septic shock, and end-stage liver disease.