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Ann Rheum Dis 65:iii29-iii33 doi:10.1136/ard.2006.058529
  • Animal models

Potential new targets in arthritis therapy: interleukin (IL)-17 and its relation to tumour necrosis factor and IL-1 in experimental arthritis

  1. M I Koenders,
  2. L A B Joosten,
  3. W B van den Berg
  1. Radboud University Nijmegen Medical Center, Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, Nijmegen, the Netherlands
  1. Correspondence to:
    M I Koenders
    Radboud University Nijmegen Medical Center, Department of Rheumatology, Rheumatology Research and Advanced Therapeutics, 272, Geert Grooteplein 26, PO Box 9101, 6500 HB Nijmegen, the Netherlands; m.koenders{at}reuma.umcn.nl

    Abstract

    Rheumatoid arthritis (RA) is a systemic autoimmune disease characterised by chronic joint inflammation and destruction. Interleukin (IL)-17 is a T cell cytokine expressed in the synovium and synovial fluid of patients with RA. IL-17 is a potent inducer of various cytokines such as tumour necrosis factor (TNF) and IL-1. IL-17 has been shown to have additive or even synergistic effects with TNF and IL-1 during the induction of cytokine expression and joint damage in vitro and in vivo. TNFα and IL-1 are considered powerful targets in the treatment of RA because of their leading role in driving the enhanced production of cytokines, chemokines, and degradative enzymes. Besides anti-TNF and anti-IL-1 therapies, whose clinical efficacy is now established, new targets have been proposed for RA which is not responding to conventional treatments. This paper discusses the role of IL-17 in experimental arthritis and its interrelationship with TNF and IL-1, currently the most targeted cytokines in the treatment of RA. IL-17 is involved in both initiation and progression of murine experimental arthritis. Studies have shown that IL-17 not only synergises with TNF, but also enhances inflammation and destruction independent of IL-1 and TNF. On the basis of these studies, the authors propose IL-17 as an interesting additional target in the treatment of RA.

    Footnotes

    • This work was supported by the Dutch Arthritis Association (grant NR 00-1-302), and by a grant of Novartis Pharma AG, Basel, Switzerland.

    • Competing interests: none declared