Targeting IL-23 and Th17-cytokines in inflammatory bowel diseases

Curr Pharm Des. 2010;16(33):3656-60. doi: 10.2174/138161210794079164.


Over the last 15 years, the use of various biological therapies has largely improved the way we manage patients with Inflammatory Bowel Diseases (IBDs). Blockade of cytokine synthesis and/or activity is at the forefront of this new era with the success of inhibitors of tumor necrosis factor (TNF)-α. These therapies are however not effective in all IBD patients and efficacy may wane. Moreover, patients treated with anti-TNF-α antibodies can develop severe side-effects and new immune-mediated diseases. Therefore, a new challenge is to elucidate new inflammatory networks in the IBD tissue and develop novel anti-cytokine compounds, which may act in patients who are resistant to or cannot receive anti-TNF-α therapies. In this article we review the available data supporting the pathogenic role of IL-23 and Th17-related cytokines in IBD, and discuss whether and how compounds that control the activity of these cytokines may enter into the therapeutic armamentarium of IBD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / metabolism
  • Crohn Disease / drug therapy
  • Crohn Disease / metabolism
  • Cytokines / antagonists & inhibitors*
  • Cytokines / metabolism
  • Humans
  • Inflammatory Bowel Diseases / drug therapy*
  • Inflammatory Bowel Diseases / metabolism
  • Interleukin-17 / antagonists & inhibitors
  • Interleukin-17 / metabolism
  • Interleukin-23 / antagonists & inhibitors*
  • Interleukin-23 / metabolism
  • Interleukins / agonists
  • Interleukins / metabolism
  • Molecular Targeted Therapy
  • Th17 Cells / drug effects*
  • Th17 Cells / metabolism*


  • Cytokines
  • IL17A protein, human
  • Interleukin-17
  • Interleukin-23
  • Interleukins
  • interleukin-22