[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 C1q knock-out mice suggest an important role of C1q in the clearance of apoptotic cell material. In addition, there are several links between C1q and SLE: Most the patients with C1q deficiency develop a SLE-like syndrome. SLE itself often causes secondary C1q deficiency and autoantibodies to C1q are detected in almost all patients with active lupus nephritis. These observations suggest a central role of C1q in apoptosis and in the pathogenesis of SLE.
Medizinische Klinik B Kantonsspital Basel Stadt. trendelenbur@ubaclu.unibas.ch
M
M
Trendelenburg
J A
JA
Schifferli
D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood*; D001327:Autoimmune Diseases / Q000276:immunology*; D015922:Complement C1q / Q000276:immunology* / Q000502:physiology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout
D001323:Autoantibodies; D015922:Complement C1q