[Progress on relationship between IL-23/IL-17 axis and inflammatory bowel disease].

Chronic inflammatory damage of intestinal mucosa is an important characteristic of inflammatory bowel disease (IBD). Studies have shown that the interleukin 23 (IL-23)/IL-17 axis is involved in intestinal mucosal inflammatory injury and plays a crucial role in the development and prognosis of IBD. IL-23 is one of the upstream molecules of IL-17, which can promote Th17 cell activation, proliferation and the secretion of inflammatory cytokines. Moreover, IL-23 is involved in the inflammatory response process of various immune cells such as neutrophils, macrophages, regulatory T cells (Tregs), the group 3 innate lymphocytes (ILC3) during IBD. Previous studies demonstrated that IL-23 and IL-17 increased in IBD, which lead to an imbalance between Tregs and auto-reactive T cells to exacerbate the inflammatory pathological damage of the intestinal mucosa. Notably, although IL-23/IL-17 is potential therapeutic target for inflammation-related diseases and anti-IL-23 strategies has proven to be effective in treating IBD, the strategy of blocking IL-17 to treat IBD has failed. Therefore, a deep understanding of the relationship between IL-17/IL-23 axis and IBD is necessary for the study of IBD treatment.