2. Defective clearance of apoptotic cells and SLE-like autoimmunity was found to be associated C1q deficiency. C1q mice developed systemic autoimmunity spontaneously, with a marked excess of free, non-ingested apoptotic cells of the kidney. Although congenital deficiency of complement cascade is rare in humans, nearly all patients who were deficient in C1q developed SLE-like disease. In both human and mice, inflammatory macrophages had defect in the uptake of apoptotic cells and the defect could be rescued by adding exogenous C1q.