Apoptosis and C1q: possible explanations for the pathogenesis of systemic lupus erythematosus

Dysregulation of apoptosis may play a major role in the pathogenesis of systemic lupus erythematosus (SLE). A defective clearance of apoptotic cells or inappropriately high rates of apoptosis may lead to a pathologic accumulation of abnormal cell material with a secondary autoimmune response. Experimental findings in apoptotic keratinocytes and Clq knock-out mice suggest an important role of Clq in the clearance of apoptotic cell material. In addition, there are several links between Clq and SLE: Most the patients with Clq deficiency develop a SLE-like syndrome. SLE itself often causes secondary Clq deficiency and autoantibodies to Clq are detected in almost all patients with active lupus nephritis. These observations suggest a central role of Clq in apoptosis and in the pathogenesis of SLE.