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Rheumatoid arthritis and the complement system

På svenska

Author

  • Marcin Okroj
  • Dick Heinegård
  • Rikard Holmdahl
  • Anna Blom

Summary, in English

Complement activation contributes to a pathological process in a number of autoimmune and inflammatory diseases, including rheumatoid arthritis (RA). In this review we summarize current knowledge of complement contribution to RA, based on clinical observations in patients and in vivo animal models, as well as on experiments in vitro aiming at elucidation of underlying molecular mechanisms. There is strong evidence that both the classical and the alternative pathways of complement are pathologically activated during RA as well as in animal models for RA. The classical pathway can be initiated by several triggers present in the inflamed joint such as deposited autoantibodies, dying cells, and exposed cartilage proteins such as fibromodulin. B cells producing autoantibodies, which in turn form immune complexes, contribute to RA pathogenesis partly via activation of complement. It appears that anaphylatoxin C5a is the main product of complement activation responsible for tissue damage in RA although deposition of membrane attack complex as well as opsonization with fragments of C3b are also important. Success of complement inhibition in the experimental models described so far encourages novel therapeutic approaches to the treatment of human RA.

Publishing year

2007

Language

English

Pages

517-530

Publication/Series

Annals of Medicine

Volume

39

Issue

7

Document type

Journal article

Publisher

Taylor & Francis

Topic

  • Rheumatology and Autoimmunity
  • Other Basic Medicine

Status

Published

Research group

  • Protein Chemistry, Malmö
  • Immunology

ISBN/ISSN/Other

  • ISSN: 1365-2060