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.
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- AIA, antigen induced arthritis
- CIA, collagen induced arthritis
- IL, interleukin
- IL-1Ra, IL-1 receptor antagonist
- MMP, matrix metalloproteinase
- RA, rheumatoid arthritis
- RANKL, receptor activator of nuclear factor κB ligand
- SCW, streptococcal cell wall
- TNF, tumour necrosis factor
- Th, T helper
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
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