Can IL-23 be a good target for ulcerative colitis?

Best Pract Res Clin Gastroenterol. 2018 Feb-Apr:32-33:95-102. doi: 10.1016/j.bpg.2018.05.016. Epub 2018 May 23.

Abstract

A considerable percentage of patients with ulcerative colitis (UC) do not respond to therapies, including anti-tumor necrosis factor (TNF) drugs and vedolizumab, or lose response over time. Hence the continuing need to find new therapeutic strategies and novel drugs to control this chronic debilitating disease. Increased levels of interleukin (IL)-23 and T helper (Th) 17 cell cytokines have been found in intestinal mucosa, plasma, and serum of patients with inflammatory bowel disease (IBD). IL23-blocking has been shown to reduce the severity of inflammation in experimental colitis. Lastly, ustekinumab, a monoclonal antibody (mAb) to the p40 subunit of IL-12 and IL-23, has showed good efficacy and safety profile in patients with Crohn's disease (CD). This review aims to discuss the available data on IL-23 and Th17 cell pathways in UC, in order to define the role of IL-23 as possible target for the treatment of UC.

Keywords: Crohn's disease; IL-23; Inflammatory bowel disease; Monoclonal antibody anti-IL23; Th17 cell pathway cytokines; Ulcerative colitis.

Publication types

  • Review

MeSH terms

  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / pathology
  • Colitis, Ulcerative / therapy*
  • Humans
  • Interleukin-23 Subunit p19 / genetics*
  • Interleukin-23 Subunit p19 / metabolism

Substances

  • IL23A protein, human
  • Interleukin-23 Subunit p19