IL-17 as a future therapeutic target for rheumatoid arthritis

Nat Rev Rheumatol. 2009 Oct;5(10):549-53. doi: 10.1038/nrrheum.2009.179.


The discovery of interleukin (IL)-17 and its major cell source, the type 17 T-helper (TH17) lymphocyte, has been a major step in the understanding of erosive arthritis. This Review summarizes current knowledge of the role of IL-17 in this context derived from both animal models and studies in patients with rheumatoid arthritis. Evidence shows that IL-17 is present at sites of inflammatory arthritis and that, in synergistic interactions, it amplifies the inflammation induced by other cytokines, primarily tumor necrosis factor. In several animal models of arthritis, inhibition of IL-17 limits inflammation and joint erosion. Initial observations from phase I trials show that signs and symptoms of RA are significantly suppressed following treatment with anti-IL-17 antibodies, without notable adverse effects. The emergence of IL-17 blockade as a future therapy in rheumatoid arthritis is highlighted, along with the potential goals and limitations of this therapeutic approach.

Publication types

  • Review

MeSH terms

  • Animals
  • Antirheumatic Agents / therapeutic use*
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / immunology*
  • Arthritis, Rheumatoid / pathology
  • Clinical Trials, Phase I as Topic
  • Disease Models, Animal
  • Drug Delivery Systems
  • Humans
  • Interleukin-17 / antagonists & inhibitors
  • Interleukin-17 / physiology*
  • Joints / immunology
  • Joints / pathology
  • Synovial Membrane / metabolism
  • Synovial Membrane / pathology
  • Th1 Cells / immunology


  • Antirheumatic Agents
  • Interleukin-17