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肠簇细胞、ILC2 与肥胖之间可能存在联系。

Possible connection between intestinal tuft cells, ILC2s and obesity.

机构信息

Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.

出版信息

Front Immunol. 2024 Jan 12;14:1266667. doi: 10.3389/fimmu.2023.1266667. eCollection 2023.

DOI:10.3389/fimmu.2023.1266667
PMID:38283340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10811205/
Abstract

Intestinal tuft cells (TCs) are defined as chemosensory cells that can "taste" danger and induce immune responses. They play a critical role in gastrointestinal parasite invasion, inflammatory bowel diseases and high-fat diet-induced obesity. Intestinal IL-25, the unique product of TCs, is a key activator of type 2 immunity, especially to promote group 2 innate lymphoid cells (ILC2s) to secret IL-13. Then the IL-13 mainly promotes intestinal stem cell (ISCs) proliferation into TCs and goblet cells. This pathway formulates the circuit in the intestine. This paper focuses on the potential role of the intestinal TC, ILC2 and their circuit in obesity-induced intestinal damage, and discussion on further study and the potential therapeutic target in obesity.

摘要

肠簇细胞(TCs)被定义为能够“感知”危险并诱导免疫反应的化学感觉细胞。它们在胃肠道寄生虫入侵、炎症性肠病和高脂肪饮食诱导的肥胖中发挥着关键作用。肠道白介素 25(IL-25)是 TCs 的独特产物,是 2 型免疫的关键激活剂,特别是促进 2 型固有淋巴细胞(ILC2)分泌白介素 13(IL-13)。然后,IL-13 主要促进肠干细胞(ISCs)增殖为 TCs 和杯状细胞。该途径在肠道中形成了一个回路。本文重点介绍了肠道 TC、ILC2 及其回路在肥胖诱导的肠道损伤中的潜在作用,并讨论了进一步研究和肥胖潜在治疗靶点的问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d9/10811205/bed5eeae8b17/fimmu-14-1266667-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d9/10811205/73d6dbedfc8b/fimmu-14-1266667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d9/10811205/bed5eeae8b17/fimmu-14-1266667-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d9/10811205/73d6dbedfc8b/fimmu-14-1266667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d9/10811205/bed5eeae8b17/fimmu-14-1266667-g002.jpg

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本文引用的文献

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Tuft cell-derived acetylcholine promotes epithelial chloride secretion and intestinal helminth clearance.微绒毛细胞衍生的乙酰胆碱促进上皮氯离子分泌和肠道寄生虫清除。
Immunity. 2024 Jun 11;57(6):1243-1259.e8. doi: 10.1016/j.immuni.2024.03.023. Epub 2024 May 13.
2
Succinate signaling attenuates high-fat diet-induced metabolic disturbance and intestinal barrier dysfunction.琥珀酸信号减弱高脂肪饮食诱导的代谢紊乱和肠道屏障功能障碍。
Pharmacol Res. 2023 Aug;194:106865. doi: 10.1016/j.phrs.2023.106865. Epub 2023 Jul 22.
3
Activating transcription factor 5 (ATF5) controls intestinal tuft and goblet cell expansion upon succinate-induced type 2 immune responses in mice.
激活转录因子 5(ATF5)控制小鼠琥珀酸诱导的 2 型免疫反应时肠道微绒毛和杯状细胞的扩增。
Cell Tissue Res. 2023 Aug;393(2):343-355. doi: 10.1007/s00441-023-03781-7. Epub 2023 May 31.
4
ILC2 require cell-intrinsic ST2 signals to promote type 2 immune responses.ILC2 需要细胞内固有 ST2 信号来促进 2 型免疫反应。
Front Immunol. 2023 Mar 31;14:1130933. doi: 10.3389/fimmu.2023.1130933. eCollection 2023.
5
Global human obesity and global social index: Relationship and clustering.全球人类肥胖与全球社会指数:关系与聚类
Front Nutr. 2023 Mar 9;10:1150403. doi: 10.3389/fnut.2023.1150403. eCollection 2023.
6
Exogenous succinate impacts mouse brown adipose tissue mitochondrial proteome and potentiates body mass reduction induced by liraglutide.外源性琥珀酸影响小鼠棕色脂肪组织线粒体蛋白质组并增强利拉鲁肽诱导的体重减轻。
Am J Physiol Endocrinol Metab. 2023 Mar 1;324(3):E226-E240. doi: 10.1152/ajpendo.00231.2022. Epub 2023 Feb 1.
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