Mitochondrial mechanisms in Treg cell regulation: Implications for immunotherapy and disease treatment

IF 3.9 3区 生物学 Q2 CELL BIOLOGY Mitochondrion Pub Date : 2024-11-02 DOI:10.1016/j.mito.2024.101975
Xiaozhen Zhao, Junmei Zhang, Caifeng Li, Weiying Kuang, Jianghong Deng, Xiaohua Tan, Chao Li, Shipeng Li
{"title":"Mitochondrial mechanisms in Treg cell regulation: Implications for immunotherapy and disease treatment","authors":"Xiaozhen Zhao,&nbsp;Junmei Zhang,&nbsp;Caifeng Li,&nbsp;Weiying Kuang,&nbsp;Jianghong Deng,&nbsp;Xiaohua Tan,&nbsp;Chao Li,&nbsp;Shipeng Li","doi":"10.1016/j.mito.2024.101975","DOIUrl":null,"url":null,"abstract":"<div><div>Regulatory T cells (Tregs) play a critical role in maintaining immune homeostasis and preventing autoimmune diseases. Recent advances in immunometabolism have revealed the pivotal role of mitochondrial dynamics and metabolism in shaping Treg functionality. Tregs depend on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to support their suppressive functions and long-term survival. Mitochondrial processes such as fusion and fission significantly influence Treg activity, with mitochondrial fusion enhancing bioenergetic efficiency and reducing reactive oxygen species (ROS) production, thereby promoting Treg stability. In contrast, excessive mitochondrial fission disrupts ATP synthesis and elevates ROS levels, impairing Treg suppressive capacity. Furthermore, mitochondrial ROS act as critical signaling molecules in Treg regulation, where controlled levels stabilize FoxP3 expression, but excessive ROS leads to mitochondrial dysfunction and immune dysregulation. Mitophagy, as part of mitochondrial quality control, also plays an essential role in preserving Treg function. Understanding the intricate interplay between mitochondrial dynamics and Treg metabolism provides valuable insights for developing novel therapeutic strategies to treat autoimmune disorders and enhance immunotherapy in cancer.</div></div>","PeriodicalId":18606,"journal":{"name":"Mitochondrion","volume":"80 ","pages":"Article 101975"},"PeriodicalIF":3.9000,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mitochondrion","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567724924001338","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Regulatory T cells (Tregs) play a critical role in maintaining immune homeostasis and preventing autoimmune diseases. Recent advances in immunometabolism have revealed the pivotal role of mitochondrial dynamics and metabolism in shaping Treg functionality. Tregs depend on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) to support their suppressive functions and long-term survival. Mitochondrial processes such as fusion and fission significantly influence Treg activity, with mitochondrial fusion enhancing bioenergetic efficiency and reducing reactive oxygen species (ROS) production, thereby promoting Treg stability. In contrast, excessive mitochondrial fission disrupts ATP synthesis and elevates ROS levels, impairing Treg suppressive capacity. Furthermore, mitochondrial ROS act as critical signaling molecules in Treg regulation, where controlled levels stabilize FoxP3 expression, but excessive ROS leads to mitochondrial dysfunction and immune dysregulation. Mitophagy, as part of mitochondrial quality control, also plays an essential role in preserving Treg function. Understanding the intricate interplay between mitochondrial dynamics and Treg metabolism provides valuable insights for developing novel therapeutic strategies to treat autoimmune disorders and enhance immunotherapy in cancer.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
调节 Treg 细胞的线粒体机制:对免疫疗法和疾病治疗的影响。
调节性 T 细胞(Tregs)在维持免疫平衡和预防自身免疫性疾病方面发挥着至关重要的作用。免疫代谢的最新进展揭示了线粒体动力学和新陈代谢在塑造 Treg 功能方面的关键作用。Tregs 依靠氧化磷酸化(OXPHOS)和脂肪酸氧化(FAO)来支持其抑制功能和长期存活。线粒体的融合和分裂等过程对 Treg 的活性有重大影响,线粒体融合可提高生物能效率,减少活性氧(ROS)的产生,从而促进 Treg 的稳定性。相反,线粒体过度裂变会破坏 ATP 合成并提高 ROS 水平,从而损害 Treg 的抑制能力。此外,线粒体 ROS 是调节 Treg 的关键信号分子,控制其水平可稳定 FoxP3 的表达,但过量的 ROS 会导致线粒体功能障碍和免疫失调。作为线粒体质量控制的一部分,线粒体吞噬在维护 Treg 功能方面也发挥着至关重要的作用。了解线粒体动力学与 Treg 新陈代谢之间错综复杂的相互作用为开发治疗自身免疫性疾病的新型治疗策略和加强癌症免疫疗法提供了宝贵的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
期刊最新文献
Scientific investigation of non-coding RNAs in mitochondrial epigenetic and aging disorders: Current nanoengineered approaches for their therapeutic improvement The multifaceted modulation of mitochondrial metabolism in tumorigenesis Impact of missense mutations on the structure–function relationship of human succinyl-CoA synthetase using in silico analysis Mitochondrial mechanisms in Treg cell regulation: Implications for immunotherapy and disease treatment Editorial Board
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1