Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
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E primary complement defects such as complete deficiency of the early components of classical complement pathway genes (C1q, C1r/s, C2, C4A and C4B) are strongly associated with increased susceptibility to SLE [61?64]. The occurrence of a lupus-like syndrome or SLE has been demonstrated in 90 of homozygous C1q deficient cases, in more than 50 of cases with C1s/C1r deficiencies, in 10 to 30 of C
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