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This article is part of the supplement: The Scientific Basis of Rheumatology

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Complement and systemic lupus erythematosus

Mark J Walport

Author affiliations

Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK

Citation and License

Arthritis Res 2002, 4(Suppl 3):S279-S293  doi:10.1186/ar586

London, UK. 24-26 June 2002

Published: 9 May 2002


Complement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Complement proteins are deposited in inflamed tissues and, in experimental models, inhibition of C5 ameliorates disease in a murine model. As a further twist to the associations between the complement system and SLE, autoantibodies to some complement proteins, especially to C1q, develop as part of the autoantibody response. The presence of anti-C1q autoantibodies is associated with severe illness, including glomerulonephritis. In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus.

C1q; complement; glomerulonephritis; lupus; SLE