Jiang Ping, Zheng Chang, Xiang Ying, Malik Sara, Su Dan, Xu Guifang, Zhang Mingming
Department of Gastroenterology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing 210093, China.
Northwestern University Feinberg School of Medicine, Chicago 60611, IL, USA.
Cytokine Growth Factor Rev. 2023 Feb;69:28-42. doi: 10.1016/j.cytogfr.2022.07.005. Epub 2022 Jul 19.
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.
炎症性肠病（IBD）的发病机制仍不清楚。免疫功能障碍可能在IBD的发病机制中起关键作用，其中CD4辅助性T（Th）细胞的作用尤为重要。Th17细胞是CD4 T细胞的主要组成部分，其分化受多种细胞外信号、转录因子、RNA和翻译后修饰的调节。Th17细胞特异性产生白细胞介素-17，并在保护黏膜和上皮组织免受细胞外微生物感染中发挥重要作用。然而，当免疫调节功能失调时，Th17细胞异常增殖并产生大量促炎细胞因子，可招募其他炎症细胞，共同诱导异常免疫反应，导致许多自身免疫性疾病的发生。近年来，研究证实Th17细胞在IBD的发病机制中起重要作用，这使其成为IBD治疗的一个可能靶点。本文综述了Th17细胞参与IBD发病机制及其靶向治疗的最新进展。
