[Pathogenesis of systemic lupus erythematosus (SLE)--the central role of complement]

Abstract

The traditional view of the pathogenesis of SLE is that immune complexes containing autoantigens and autoantibodies activate complement, and that this causes inflammatory injury to tissues. Although this model is biologically plausible, it cannot account for all of the clinical observations that link the complement system and SLE. In particular, the observation that complement deficiency causes lupus is hard to reconcile with the concept that complement activation products are the major cause of inflammatory injury in the disease. More recent data suggests that the role of complement in SLE is rather protective. Bindung of complement might prevent an autoimmune response by supporting the clearance of immuncomplexes and apoptotic cell debrid.