Immunosenescence in autoimmune diseases

IF 9.2 1区医学 Q1 IMMUNOLOGY

Autoimmunity reviews Pub Date : 2025-03-23 DOI:10.1016/j.autrev.2025.103805

Huifang Hu , Guangyue Zhang , Tao Chen , Yi Liu , Liesu Meng , Rikard Holmdahl , Lunzhi Dai , Yi Zhao

{"title":"Immunosenescence in autoimmune diseases","authors":"Huifang Hu , Guangyue Zhang , Tao Chen , Yi Liu , Liesu Meng , Rikard Holmdahl , Lunzhi Dai , Yi Zhao","doi":"10.1016/j.autrev.2025.103805","DOIUrl":null,"url":null,"abstract":"<div><div>Autoimmune diseases (AIDs) are a group of disorders in which the immune system mistakenly attacks the body's own tissues, characterized by the loss of tolerance to self-antigens and destruction of tissues. Aging is a natural process of physiological decline that also alters the immune system, a condition known as immunosenescence. During immunosenescence, the immune system undergoes various changes, including modifications and antigenicity of self-antigens, abnormalities in the quantity, phenotype, and function of lymphocytes and antibodies, as well as a narrowing of the B and T cell receptor repertoire, changes that may increase susceptibility to AIDs. Additionally, senescent immune cells and the senescence-associated secretory phenotype (SASP) contribute to target organ involvement in AIDs, exacerbating chronic inflammation and tissue damage. Mitochondrial dysfunction and metabolic imbalances in AIDs lead to the accumulation of senescent cells, which act as upstream drivers of immunosenescence. In this review, we summarize the bidirectional relationship between AIDs and immunosenescence, as well as its potential mechanisms. Therapeutic approaches targeting immunosenescence in AIDs remain at an early stage. Strategies aimed at resetting or reversing the aging immune system are expected to become a novel direction in the future.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 6","pages":"Article 103805"},"PeriodicalIF":9.2000,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autoimmunity reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1568997225000655","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

Abstract

Autoimmune diseases (AIDs) are a group of disorders in which the immune system mistakenly attacks the body's own tissues, characterized by the loss of tolerance to self-antigens and destruction of tissues. Aging is a natural process of physiological decline that also alters the immune system, a condition known as immunosenescence. During immunosenescence, the immune system undergoes various changes, including modifications and antigenicity of self-antigens, abnormalities in the quantity, phenotype, and function of lymphocytes and antibodies, as well as a narrowing of the B and T cell receptor repertoire, changes that may increase susceptibility to AIDs. Additionally, senescent immune cells and the senescence-associated secretory phenotype (SASP) contribute to target organ involvement in AIDs, exacerbating chronic inflammation and tissue damage. Mitochondrial dysfunction and metabolic imbalances in AIDs lead to the accumulation of senescent cells, which act as upstream drivers of immunosenescence. In this review, we summarize the bidirectional relationship between AIDs and immunosenescence, as well as its potential mechanisms. Therapeutic approaches targeting immunosenescence in AIDs remain at an early stage. Strategies aimed at resetting or reversing the aging immune system are expected to become a novel direction in the future.

查看原文本刊更多论文

自身免疫性疾病中的免疫衰老

自身免疫性疾病（艾滋病）是免疫系统错误地攻击人体自身组织的一组疾病，其特征是对自身抗原失去耐受性和组织破坏。衰老是一种生理衰退的自然过程，也会改变免疫系统，这种情况被称为免疫衰老。在免疫衰老期间，免疫系统会发生各种变化，包括自身抗原的修饰和抗原性，淋巴细胞和抗体数量、表型和功能的异常，以及B细胞和T细胞受体库的变窄，这些变化可能会增加对艾滋病的易感性。此外，衰老的免疫细胞和衰老相关的分泌表型（SASP）有助于艾滋病的靶器官受累，加剧慢性炎症和组织损伤。艾滋病的线粒体功能障碍和代谢失衡导致衰老细胞的积累，这是免疫衰老的上游驱动因素。本文就艾滋病与免疫衰老的双向关系及其可能的机制进行综述。针对艾滋病免疫衰老的治疗方法仍处于早期阶段。旨在重新设置或逆转老化免疫系统的策略有望成为未来的新方向。

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分钟内获得全文求助全文

来源期刊

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.