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Published in: Arthritis Research & Therapy 3/2002

01-07-2002 | Review

Complement and systemic lupus erythematosus

Author: Mark J Walport

Published in: Arthritis Research & Therapy | Special Issue 3/2002

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Chapter summary

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.
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Metadata
Title
Complement and systemic lupus erythematosus
Author
Mark J Walport
Publication date
01-07-2002
Publisher
BioMed Central
Published in
Arthritis Research & Therapy / Issue Special Issue 3/2002
Electronic ISSN: 1478-6362
DOI
https://doi.org/10.1186/ar586

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