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

Area of Science:

• Immunology
• Gastroenterology

Background:

• Chronic inflammation of the intestinal mucosa characterizes inflammatory bowel disease (IBD).
• The interleukin 23 (IL-23)/IL-17 signaling pathway is implicated in intestinal mucosal inflammatory injury and IBD pathogenesis.
• IL-23, an upstream regulator of IL-17, promotes Th17 cell activation and inflammatory cytokine secretion, impacting various immune cells in IBD.

Purpose of the Study:

• To elucidate the intricate relationship between the IL-23/IL-17 axis and inflammatory bowel disease (IBD).
• To understand the differential therapeutic efficacy of targeting IL-23 versus IL-17 in IBD.

Main Methods:

• Review of existing literature on the IL-23/IL-17 axis in IBD.
• Analysis of immune cell involvement (Th17, neutrophils, macrophages, Tregs, ILC3) in IBD pathogenesis.
• Comparison of therapeutic strategies targeting IL-23 and IL-17 in preclinical and clinical settings.

Main Results:

• Elevated levels of IL-23 and IL-17 are observed in IBD patients.
• The IL-23/IL-17 axis contributes to Treg/auto-reactive T cell imbalance, exacerbating intestinal inflammation.
• Anti-IL-23 therapies have demonstrated efficacy in treating IBD, whereas anti-IL-17 strategies have shown limited success.

Conclusions:

• The IL-23/IL-17 axis is a critical factor in the inflammatory processes of IBD.
• Targeting IL-23 represents a viable therapeutic strategy for IBD, contrasting with the limited efficacy of IL-17 blockade.
• Further research into the IL-23/IL-17 axis is essential for advancing IBD treatment strategies.