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辅助性 T 细胞 17 在炎症性肠病中的作用及研究进展。

The role of Th17 cells in inflammatory bowel disease and the research progress.

机构信息

Department of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, China.

出版信息

Front Immunol. 2023 Jan 9;13:1055914. doi: 10.3389/fimmu.2022.1055914. eCollection 2022.

DOI:10.3389/fimmu.2022.1055914
PMID:36700221
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9870314/
Abstract

Th17 cells play an important role in the abnormal immune response in inflammatory bowel disease (IBD) and are involved in the development and progression of inflammation and fibrosis. An increasing amount of data has shown that gut microbes are important parts of intestinal immunity and regulators of Th17 cellular immunity. Th17 cell differentiation is regulated by intestinal bacteria and cytokines, and Th17 cells regulate the intestinal mucosal immune microenvironment by secreting cytokines, such as IL-17, IL-21, and IL-26. Solid evidence showed that, regarding the treatment of IBD by targeting Th17 cells, the therapeutic effect of different biological agents varies greatly. Fecal bacteria transplantation (FMT) in the treatment of IBD has been a popular research topic in recent years and is safe and effective with few side effects. To further understand the role of Th17 cells in the progression of IBD and associated therapeutic prospects, this review will discuss the progress of related research on Th17 cells in IBD by focusing on the interaction and immune regulation between Th17 cells and gut microbiota.

摘要

Th17 细胞在炎症性肠病（IBD）中的异常免疫反应中发挥重要作用，并参与炎症和纤维化的发展和进展。越来越多的数据表明，肠道微生物是肠道免疫的重要组成部分，也是 Th17 细胞免疫的调节剂。Th17 细胞的分化受肠道细菌和细胞因子的调节，Th17 细胞通过分泌细胞因子如 IL-17、IL-21 和 IL-26 来调节肠道黏膜免疫微环境。有确凿证据表明，针对 Th17 细胞治疗 IBD，不同生物制剂的治疗效果差异很大。粪便细菌移植（FMT）治疗 IBD 是近年来的热门研究课题，具有安全有效、副作用少的特点。为了进一步了解 Th17 细胞在 IBD 进展中的作用及相关治疗前景，本综述通过关注 Th17 细胞与肠道微生物群之间的相互作用和免疫调节，讨论了 Th17 细胞在 IBD 中相关研究的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/29e3a0b8343a/fimmu-13-1055914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/c5f457fa0f3a/fimmu-13-1055914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/14ad14fc4763/fimmu-13-1055914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/29e3a0b8343a/fimmu-13-1055914-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/c5f457fa0f3a/fimmu-13-1055914-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/14ad14fc4763/fimmu-13-1055914-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7822/9870314/29e3a0b8343a/fimmu-13-1055914-g003.jpg

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本文引用的文献

[1]
Excessive intake of sugar: An accomplice of inflammation.

Front Immunol. 2022

[2]
and Its Metabolite Butyrate Inhibit Colitis and Upregulate TLR5 through the SP3 Signaling Pathway.

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Biomedicines. 2022-7-19

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Therap Adv Gastroenterol. 2022-3-8

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