重塑 T 细胞线粒体代谢,治疗自身免疫性疾病。

IF 9.2 1区 医学 Q1 IMMUNOLOGY Autoimmunity reviews Pub Date : 2024-06-01 DOI:10.1016/j.autrev.2024.103583
Liyan Lin , Ruyu Ren , Qiao Xiong , Chunfu Zheng , Bin Yang , Huiqing Wang
{"title":"重塑 T 细胞线粒体代谢,治疗自身免疫性疾病。","authors":"Liyan Lin ,&nbsp;Ruyu Ren ,&nbsp;Qiao Xiong ,&nbsp;Chunfu Zheng ,&nbsp;Bin Yang ,&nbsp;Huiqing Wang","doi":"10.1016/j.autrev.2024.103583","DOIUrl":null,"url":null,"abstract":"<div><p>T cells are key drivers of the pathogenesis of autoimmune diseases by producing cytokines, stimulating the generation of autoantibodies, and mediating tissue and cell damage. Distinct mitochondrial metabolic pathways govern the direction of T-cell differentiation and function and rely on specific nutrients and metabolic enzymes. Metabolic substrate uptake and mitochondrial metabolism form the foundational elements for T-cell activation, proliferation, differentiation, and effector function, contributing to the dynamic interplay between immunological signals and mitochondrial metabolism in coordinating adaptive immunity. Perturbations in substrate availability and enzyme activity may impair T-cell immunosuppressive function, fostering autoreactive responses and disrupting immune homeostasis, ultimately contributing to autoimmune disease pathogenesis. A growing body of studies has explored how metabolic processes regulate the function of diverse T-cell subsets in autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), autoimmune hepatitis (AIH), inflammatory bowel disease (IBD), and psoriasis. This review describes the coordination of T-cell biology by mitochondrial metabolism, including the electron transport chain (ETC), oxidative phosphorylation, amino acid metabolism, fatty acid metabolism, and one‑carbon metabolism. This study elucidated the intricate crosstalk between mitochondrial metabolic programs, signal transduction pathways, and transcription factors. This review summarizes potential therapeutic targets for T-cell mitochondrial metabolism and signaling in autoimmune diseases, providing insights for future studies.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103583"},"PeriodicalIF":9.2000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568997224000740/pdfft?md5=6bb063881495178bffec26ec237556aa&pid=1-s2.0-S1568997224000740-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Remodeling of T-cell mitochondrial metabolism to treat autoimmune diseases\",\"authors\":\"Liyan Lin ,&nbsp;Ruyu Ren ,&nbsp;Qiao Xiong ,&nbsp;Chunfu Zheng ,&nbsp;Bin Yang ,&nbsp;Huiqing Wang\",\"doi\":\"10.1016/j.autrev.2024.103583\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>T cells are key drivers of the pathogenesis of autoimmune diseases by producing cytokines, stimulating the generation of autoantibodies, and mediating tissue and cell damage. Distinct mitochondrial metabolic pathways govern the direction of T-cell differentiation and function and rely on specific nutrients and metabolic enzymes. Metabolic substrate uptake and mitochondrial metabolism form the foundational elements for T-cell activation, proliferation, differentiation, and effector function, contributing to the dynamic interplay between immunological signals and mitochondrial metabolism in coordinating adaptive immunity. Perturbations in substrate availability and enzyme activity may impair T-cell immunosuppressive function, fostering autoreactive responses and disrupting immune homeostasis, ultimately contributing to autoimmune disease pathogenesis. A growing body of studies has explored how metabolic processes regulate the function of diverse T-cell subsets in autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), autoimmune hepatitis (AIH), inflammatory bowel disease (IBD), and psoriasis. This review describes the coordination of T-cell biology by mitochondrial metabolism, including the electron transport chain (ETC), oxidative phosphorylation, amino acid metabolism, fatty acid metabolism, and one‑carbon metabolism. This study elucidated the intricate crosstalk between mitochondrial metabolic programs, signal transduction pathways, and transcription factors. This review summarizes potential therapeutic targets for T-cell mitochondrial metabolism and signaling in autoimmune diseases, providing insights for future studies.</p></div>\",\"PeriodicalId\":8664,\"journal\":{\"name\":\"Autoimmunity reviews\",\"volume\":\"23 6\",\"pages\":\"Article 103583\"},\"PeriodicalIF\":9.2000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S1568997224000740/pdfft?md5=6bb063881495178bffec26ec237556aa&pid=1-s2.0-S1568997224000740-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autoimmunity reviews\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1568997224000740\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autoimmunity reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1568997224000740","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

T 细胞通过产生细胞因子、刺激自身抗体的产生以及介导组织和细胞损伤,是自身免疫性疾病发病机制的关键驱动因素。不同的线粒体代谢途径决定着 T 细胞分化和功能的方向,并依赖于特定的营养物质和代谢酶。代谢底物摄取和线粒体代谢是 T 细胞活化、增殖、分化和效应功能的基本要素,有助于免疫信号和线粒体代谢在协调适应性免疫中的动态相互作用。底物可用性和酶活性的紊乱可能会损害 T 细胞的免疫抑制功能,助长自体反应,破坏免疫平衡,最终导致自身免疫性疾病的发病。越来越多的研究探讨了新陈代谢过程如何调节系统性红斑狼疮(SLE)、多发性硬化症(MS)、自身免疫性肝炎(AIH)、炎症性肠病(IBD)和银屑病等自身免疫性疾病中不同 T 细胞亚群的功能。这篇综述介绍了线粒体代谢对 T 细胞生物学的协调作用,包括电子传递链(ETC)、氧化磷酸化、氨基酸代谢、脂肪酸代谢和一碳代谢。这项研究阐明了线粒体代谢程序、信号转导途径和转录因子之间错综复杂的相互关系。本综述总结了自身免疫性疾病中 T 细胞线粒体代谢和信号转导的潜在治疗靶点,为今后的研究提供了启示。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
Remodeling of T-cell mitochondrial metabolism to treat autoimmune diseases

T cells are key drivers of the pathogenesis of autoimmune diseases by producing cytokines, stimulating the generation of autoantibodies, and mediating tissue and cell damage. Distinct mitochondrial metabolic pathways govern the direction of T-cell differentiation and function and rely on specific nutrients and metabolic enzymes. Metabolic substrate uptake and mitochondrial metabolism form the foundational elements for T-cell activation, proliferation, differentiation, and effector function, contributing to the dynamic interplay between immunological signals and mitochondrial metabolism in coordinating adaptive immunity. Perturbations in substrate availability and enzyme activity may impair T-cell immunosuppressive function, fostering autoreactive responses and disrupting immune homeostasis, ultimately contributing to autoimmune disease pathogenesis. A growing body of studies has explored how metabolic processes regulate the function of diverse T-cell subsets in autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), autoimmune hepatitis (AIH), inflammatory bowel disease (IBD), and psoriasis. This review describes the coordination of T-cell biology by mitochondrial metabolism, including the electron transport chain (ETC), oxidative phosphorylation, amino acid metabolism, fatty acid metabolism, and one‑carbon metabolism. This study elucidated the intricate crosstalk between mitochondrial metabolic programs, signal transduction pathways, and transcription factors. This review summarizes potential therapeutic targets for T-cell mitochondrial metabolism and signaling in autoimmune diseases, providing insights for future studies.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Autoimmunity reviews
Autoimmunity reviews 医学-免疫学
CiteScore
24.70
自引率
4.40%
发文量
164
审稿时长
21 days
期刊介绍: Autoimmunity Reviews is a publication that features up-to-date, structured reviews on various topics in the field of autoimmunity. These reviews are written by renowned experts and include demonstrative illustrations and tables. Each article will have a clear "take-home" message for readers. The selection of articles is primarily done by the Editors-in-Chief, based on recommendations from the international Editorial Board. The topics covered in the articles span all areas of autoimmunology, aiming to bridge the gap between basic and clinical sciences. In terms of content, the contributions in basic sciences delve into the pathophysiology and mechanisms of autoimmune disorders, as well as genomics and proteomics. On the other hand, clinical contributions focus on diseases related to autoimmunity, novel therapies, and clinical associations. Autoimmunity Reviews is internationally recognized, and its articles are indexed and abstracted in prestigious databases such as PubMed/Medline, Science Citation Index Expanded, Biosciences Information Services, and Chemical Abstracts.
期刊最新文献
Advancing understanding of autoimmune disease-related interstitial lung disease (AD-ILD): A global perspective on research focus and future directions. Is it time for treat to target in antiphospholipid syndrome? Global research landscape on antiphospholipid syndrome and systemic lupus erythematosus: Trends, collaborations, and future directions. Reply to "Refining search and keyword strategies in autoimmune ear disease bibliometric studies". Treatment of two pediatric patients with refractory systemic lupus erythematosus using CD19-targeted CAR T cells.
×
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