Purpose of review: It is well recognized that the complement system plays multiple roles in systemic lupus erythematosus. Activation of the classical pathway by immune complexes leads to the generation of inflammatory mediators, thus promoting tissue injury. Complement activation also plays an important role in the maintenance of tolerance to self-antigens. This review discusses recent insights in the role of complement in the pathogenesis of systemic lupus erythematosus.
Recent findings: The antiphospholipid syndrome is a major feature of systemic lupus erythematosus. New findings have clearly demonstrated that the prothrombotic effects seen in a mouse model of this syndrome depend on complement activation, whereas the protective effects of heparin are due to its anticomplementary effects rather than its anticoagulant action. Secondly, a potential mechanism explaining the association of anti-C1q autoantibodies with lupus glomerulonephritis has been elucidated in a mouse model system.
Summary: New findings have helped to reinforce the role of complement in the etiology and tissue damage of systemic lupus erythematosus. These findings point to more precise, mechanism-based therapies for autoimmune and inflammatory disease.