Abstract

Deficiencies in the classical pathway of the complement system have been implicated in the etiology and pathogenesis of systemic lupus erythematosus (SLE) for several decades. Recent advances have suggested that this link is due to a critical role of complement in the recognition and clearance of the cellular remnants of apoptosis. In this review, we summarize the role of apoptosis in generation of an autoimmune response, and we integrate recent advances that link apoptosis, complement activation and the etiopathogenesis of SLE.

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