The involvement of TH17 cells in the pathogenesis of IBD

The pathogenesis of inflammatory bowel disease (IBD) is still unclear. Immune dysfunction may play a key role in the pathogenesis of IBD, in which the role of CD4+ T helper (Th) cells is particularly important. Th17 cells are a major component of CD4+ T cells, and their differentiation is regulated by a variety of extracellular signals, transcription factors, RNA, and posttranslational modifications. Th17 cells specifically produce IL-17 and play an important role in the protection of mucous membranes and epithelial tissues against infection by extracellular microbes. However, when immune regulation is dysfunctional, Th17 cells abnormally proliferate and produce large amounts of proinflammatory cytokines that can recruit other inflammatory cells, which together induce abnormal immune responses and result in the development of many autoimmune diseases. In recent years, studies have confirmed that Th17 cells play an important role in the pathogenesis of IBD, which makes it a possible target for IBD therapy. This article reviews the recent progress of Th17 cells involved in the pathogenesis of IBD and its targeted therapy.

Automated summary

The pathogenesis of inflammatory bowel disease (IBD) is still unclear and immune dysfunction might play a key role. CD4+ T helper (Th) cells are especially important in this process, with Th17 cells being a major component of CD4+ T cells. Th17 cells produce IL-17 and protect mucous membranes and epithelial tissues against infection. However, when immune regulation is dysfunctional, Th17 cells proliferate abnormally and produce large amounts of proinflammatory cytokines, leading to abnormal immune responses and the development of autoimmune diseases. Recent studies have shown the importance of Th17 cells in the pathogenesis of IBD and their potential as a target for therapy.