CBLs 下调预示着 T 细胞泛素化会导致自身免疫病

IF 6.6 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cell Chemical Biology Pub Date : 2024-07-18 DOI:10.1016/j.chembiol.2024.06.010

Aurobind Vidyarthi , Joe Craft

{"title":"CBLs 下调预示着 T 细胞泛素化会导致自身免疫病","authors":"Aurobind Vidyarthi , Joe Craft","doi":"10.1016/j.chembiol.2024.06.010","DOIUrl":null,"url":null,"abstract":"<div>In a study published in the July issue of Immunity, Li et al.1 demonstrate that expression of the E3 ubiquitin ligases CBL and CBL-B is downregulated in Tfh cells in SLE with Tfh cell expansion and autoimmunity. This leads to reduced ubiquitination of the T cell costimulator ICOS which regulates proteostasis of the Tfh cell transcription factor BCL6 via chaperone-mediated autophagy.</div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"31 7","pages":"Pages 1239-1241"},"PeriodicalIF":6.6000,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"CBLs downregulation foretells T cell ubiquitination leading to autoimmunity\",\"authors\":\"Aurobind Vidyarthi , Joe Craft\",\"doi\":\"10.1016/j.chembiol.2024.06.010\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>In a study published in the July issue of Immunity, Li et al.1 demonstrate that expression of the E3 ubiquitin ligases CBL and CBL-B is downregulated in Tfh cells in SLE with Tfh cell expansion and autoimmunity. This leads to reduced ubiquitination of the T cell costimulator ICOS which regulates proteostasis of the Tfh cell transcription factor BCL6 via chaperone-mediated autophagy.</div>\",\"PeriodicalId\":265,\"journal\":{\"name\":\"Cell Chemical Biology\",\"volume\":\"31 7\",\"pages\":\"Pages 1239-1241\"},\"PeriodicalIF\":6.6000,\"publicationDate\":\"2024-07-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Chemical Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2451945624002708\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Chemical Biology","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2451945624002708","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

摘要

在发表于《免疫》（Immunity）七月刊的一项研究中，Li 等人1 证实，在伴有 Tfh 细胞扩增和自身免疫的系统性红斑狼疮患者的 Tfh 细胞中，E3 泛素连接酶 CBL 和 CBL-B 的表达下调。这导致T细胞成本刺激因子ICOS的泛素化减少，而ICOS通过伴侣介导的自噬调节Tfh细胞转录因子BCL6的蛋白稳态。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

CBLs downregulation foretells T cell ubiquitination leading to autoimmunity

In a study published in the July issue of Immunity, Li et al.¹ demonstrate that expression of the E3 ubiquitin ligases CBL and CBL-B is downregulated in Tfh cells in SLE with Tfh cell expansion and autoimmunity. This leads to reduced ubiquitination of the T cell costimulator ICOS which regulates proteostasis of the Tfh cell transcription factor BCL6 via chaperone-mediated autophagy.

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

Cell Chemical Biology Biochemistry, Genetics and Molecular Biology-Molecular Medicine

CiteScore

14.70

自引率

2.30%

发文量

143

期刊介绍： Cell Chemical Biology, a Cell Press journal established in 1994 as Chemistry & Biology, focuses on publishing crucial advances in chemical biology research with broad appeal to our diverse community, spanning basic scientists to clinicians. Pioneering investigations at the chemistry-biology interface, the journal fosters collaboration between these disciplines. We encourage submissions providing significant conceptual advancements of broad interest across chemical, biological, clinical, and related fields. Particularly sought are articles utilizing chemical tools to perturb, visualize, and measure biological systems, offering unique insights into molecular mechanisms, disease biology, and therapeutics.