T细胞衰老:一种新的衰老治疗靶点

S. Delgado Pulido, J. I. Escrig-Larena, M. Mittelbrunn
{"title":"T细胞衰老:一种新的衰老治疗靶点","authors":"S. Delgado Pulido, J. I. Escrig-Larena, M. Mittelbrunn","doi":"10.32440/ar.2022.139.02.doc01","DOIUrl":null,"url":null,"abstract":"Aging of the immune system is characterized by a progressive loss of function, which limits vaccine effectiveness and is responsible for the increase in the susceptibility to infections, cancer and autoimmune diseases observed in elderly population. Recent evidences suggest that intrinsic alterations accumulated in T lymphocytes with age actively contribute to the state of chronic inflammation which underlies age-associated pathologies. We have accelerated the aging process in mice by inducing a mitochondrial dysfunction exclusively in T cells. These mice showed signs of systemic premature senescence and multimorbidity, evidencing that alterations in T cell functionality are sufficient to accelerate a whole-organism aging phenotype. Thus, T cell aging plays a crucial role in systemic deterioration and may be involved in neurodegenerative, cardiovascular and metabolic diseases whose incidence drastically increases with age. Understanding how the immune system contributes to age-associated multimorbidity is an urgent challenge, which could lead to the development of new therapeutic strategies destined to achieve a healthier aging. In this regard, immunotherapy is emerging as a new and promising technique aimed to delay age-associated diseases.","PeriodicalId":75487,"journal":{"name":"Anales de la Real Academia Nacional de Medicina","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"T cell senescence: A novel therapeutic target for aging\",\"authors\":\"S. Delgado Pulido, J. I. Escrig-Larena, M. Mittelbrunn\",\"doi\":\"10.32440/ar.2022.139.02.doc01\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Aging of the immune system is characterized by a progressive loss of function, which limits vaccine effectiveness and is responsible for the increase in the susceptibility to infections, cancer and autoimmune diseases observed in elderly population. Recent evidences suggest that intrinsic alterations accumulated in T lymphocytes with age actively contribute to the state of chronic inflammation which underlies age-associated pathologies. We have accelerated the aging process in mice by inducing a mitochondrial dysfunction exclusively in T cells. These mice showed signs of systemic premature senescence and multimorbidity, evidencing that alterations in T cell functionality are sufficient to accelerate a whole-organism aging phenotype. Thus, T cell aging plays a crucial role in systemic deterioration and may be involved in neurodegenerative, cardiovascular and metabolic diseases whose incidence drastically increases with age. Understanding how the immune system contributes to age-associated multimorbidity is an urgent challenge, which could lead to the development of new therapeutic strategies destined to achieve a healthier aging. In this regard, immunotherapy is emerging as a new and promising technique aimed to delay age-associated diseases.\",\"PeriodicalId\":75487,\"journal\":{\"name\":\"Anales de la Real Academia Nacional de Medicina\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Anales de la Real Academia Nacional de Medicina\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.32440/ar.2022.139.02.doc01\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anales de la Real Academia Nacional de Medicina","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32440/ar.2022.139.02.doc01","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

免疫系统的老化以功能的逐渐丧失为特征,这限制了疫苗的有效性,并导致在老年人群中观察到的感染、癌症和自身免疫性疾病的易感性增加。最近的证据表明,随着年龄的增长,T淋巴细胞中积累的内在变化积极促成了慢性炎症状态,而慢性炎症是年龄相关病理的基础。我们通过在T细胞中诱导线粒体功能障碍来加速小鼠的衰老过程。这些小鼠表现出系统性早衰和多发病的迹象,证明T细胞功能的改变足以加速整个机体的衰老表型。因此,T细胞衰老在系统性恶化中起着至关重要的作用,可能与神经退行性疾病、心血管疾病和代谢性疾病有关,这些疾病的发病率随着年龄的增长而急剧增加。了解免疫系统如何导致与年龄相关的多发病是一项紧迫的挑战,这可能会导致开发新的治疗策略,以实现更健康的衰老。在这方面,免疫疗法正在成为一种新的、有前途的技术,旨在延缓与年龄相关的疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
T cell senescence: A novel therapeutic target for aging
Aging of the immune system is characterized by a progressive loss of function, which limits vaccine effectiveness and is responsible for the increase in the susceptibility to infections, cancer and autoimmune diseases observed in elderly population. Recent evidences suggest that intrinsic alterations accumulated in T lymphocytes with age actively contribute to the state of chronic inflammation which underlies age-associated pathologies. We have accelerated the aging process in mice by inducing a mitochondrial dysfunction exclusively in T cells. These mice showed signs of systemic premature senescence and multimorbidity, evidencing that alterations in T cell functionality are sufficient to accelerate a whole-organism aging phenotype. Thus, T cell aging plays a crucial role in systemic deterioration and may be involved in neurodegenerative, cardiovascular and metabolic diseases whose incidence drastically increases with age. Understanding how the immune system contributes to age-associated multimorbidity is an urgent challenge, which could lead to the development of new therapeutic strategies destined to achieve a healthier aging. In this regard, immunotherapy is emerging as a new and promising technique aimed to delay age-associated diseases.
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
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信