Interleukin-23/Th17 pathways and inflammatory bowel disease

Inflamm Bowel Dis. 2009 Jul;15(7):1090-100. doi: 10.1002/ibd.20894.


The IL-23/Th17 pathway has recently been identified to play a critical role in a number of chronic inflammatory diseases including inflammatory bowel disease (IBD). The identification in IBD patients of associations in IL23R and regions that include other genes in the IL-23/Th17 pathway has highlighted the importance of proper IL-23/Th17 pathway regulation in intestinal immune homeostasis. IL-23 plays a role in CD4+ Th17 lineage cells, characterized by IL-17 secretion and the expression of the transcription factor retinoic acid-related orphan receptor (ROR)gamma tau, and in other immune and nonimmune cells. The balance between effector T cell subsets, such as Th17 cells, and CD4+ T regulatory subsets is finely regulated; dysregulation of this balance can lead to inflammation and autoimmunity. As such, the IL-23/Th17 pathway contributes to immune responses that play a role in defenses to microbial infection, as well as in the intestinal inflammation observed in both animal models of colitis and human IBD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • Humans
  • Inflammatory Bowel Diseases / immunology*
  • Inflammatory Bowel Diseases / metabolism*
  • Interleukin-17 / immunology
  • Interleukin-17 / metabolism*
  • Interleukin-23 / immunology
  • Interleukin-23 / metabolism*
  • Signal Transduction / immunology*


  • Interleukin-17
  • Interleukin-23