Interleukin-17 in inflammatory myopathies

Curr Rheumatol Rep. 2012 Jun;14(3):252-6. doi: 10.1007/s11926-012-0242-x.


Since the identification of interleukin (IL)-17 as a T-cell-derived cytokine 15 years ago, the contribution of the T-helper type 17 (Th17) pathway in inducing and maintaining chronic inflammation has been well-established, particularly in rheumatoid arthritis. In addition to the main Th1 profile first suggested to contribute to inflammatory myopathies, the presence in inflamed muscle tissue of myositis of IL-17-producing cells, in association with activated dendritic cells, suggests a local activation of the IL-23-Th17 pathway. IL-17 can act on muscle cells together with proinflammatory cytokines produced by monocytes and innate immunity to amplify the immune response that could lead to muscle destruction. Evidence for activation of the Th17 pathway in myositis lesions and in vitro effects of IL-17 on muscle cells suggest IL-17 as a therapeutic target. Inhibitors of IL-17 have been tested in other inflammatory conditions, but the position of IL-17 inhibition in the treatment of inflammatory myopathies remains to be defined.

Publication types

  • Review

MeSH terms

  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / immunology
  • Humans
  • Immunologic Factors / therapeutic use
  • Interleukin-17 / antagonists & inhibitors
  • Interleukin-17 / immunology*
  • Molecular Targeted Therapy / methods
  • Muscle Cells / immunology
  • Myositis / drug therapy
  • Myositis / immunology*
  • Th17 Cells / immunology


  • Immunologic Factors
  • Interleukin-17