The IL-23/IL-17 axis in inflammation

J Clin Invest. 2006 May;116(5):1218-22. doi: 10.1172/JCI28508.


IL-23 induces the differentiation of naive CD4(+) T cells into highly pathogenic helper T cells (Th17/Th(IL-17)) that produce IL-17, IL-17F, IL-6, and TNF-alpha, but not IFN-gamma and IL-4. Two studies in this issue of the JCI demonstrate that blocking IL-23 or its downstream factors IL-17 and IL-6, but not the IL-12/IFN-gamma pathways, can significantly suppress disease development in animal models of inflammatory bowel disease and MS (see the related articles beginning on pages 1310 and 1317). These studies suggest that the IL-23/IL-17 pathway may be a novel therapeutic target for the treatment of chronic inflammatory diseases.

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / cytology
  • Disease Models, Animal
  • Humans
  • Inflammation*
  • Inflammatory Bowel Diseases / pathology
  • Interferon-gamma / metabolism
  • Interleukin-17 / physiology*
  • Interleukin-23
  • Interleukin-23 Subunit p19
  • Interleukin-4 / metabolism
  • Interleukins / physiology*
  • Models, Biological
  • Multiple Sclerosis / pathology
  • T-Lymphocytes, Helper-Inducer / cytology


  • IL23A protein, human
  • Interleukin-17
  • Interleukin-23
  • Interleukin-23 Subunit p19
  • Interleukins
  • Interleukin-4
  • Interferon-gamma