肠道 TH17 细胞的氧化应激使小鼠易受细菌感染。

Immunometabolism (Cobham (Surrey, England)) Pub Date : 2024-11-13 eCollection Date: 2024-10-01 DOI:10.1097/IN9.0000000000000049
Simon O'Shaughnessy, David K Finlay
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引用次数: 0

摘要

德克-布伦纳(Dirk Brenner)实验室最近在 2024 年 8 月的《细胞代谢》(Cell Metabolism)杂志上发表了一篇论文,强调了有效管理肠道 TH17 T 细胞中活性氧(ROS)对最大限度地减少肠道细菌感染造成的损害的重要性。这篇评论将讨论谷胱甘肽对细胞 ROS 的控制,以及人们逐渐认识到中和免疫细胞中的 ROS 对不同免疫亚群的个性化功能至关重要。在本研究中,肠道中 TH17 细胞内的 ROS 管理被证明对维持 IL22 细胞因子的产生至关重要,从而在应对细菌感染时维持肠道平衡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress in gut TH17 cells makes mice susceptible to bacterial infection.

A recent paper published in Cell Metabolism in August 2024 by Dirk Brenner's laboratory highlights the importance of effectively managing reactive oxygen species (ROS) in gut TH17 T cells for minimizing the damage caused by intestinal bacterial infection. This commentary will discuss the control of cellular ROS by glutathione and the emerging understanding that neutralizing ROS in immune cells is essential for the individualized functions of different immune subsets. In the case of this study, managing ROS within TH17 cells in the gut was shown to be essential to sustain the production of IL22 cytokine to maintain gut homeostasis in response to bacterial infection.

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