{"title":"干扰素通过 CXCL13 破坏系统性红斑狼疮的免疫和组织稳态","authors":"Mehrdad Pazhouhandeh, Di Yu","doi":"10.1038/s41584-024-01164-y","DOIUrl":null,"url":null,"abstract":"Type I interferon has a crucial role in the immunopathogenesis of systemic lupus erythematosus (SLE). Analysis of CD4+ T cells from individuals with SLE now shows that type I interferon intervenes with the transcriptional regulators AHR and JUN to downregulate expression of IL-22, which promotes tissue regeneration, and upregulate the expression of CXCL13, which supports lymphoid structure formation.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4000,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Interferon disrupts immune and tissue homeostasis in SLE via CXCL13\",\"authors\":\"Mehrdad Pazhouhandeh, Di Yu\",\"doi\":\"10.1038/s41584-024-01164-y\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Type I interferon has a crucial role in the immunopathogenesis of systemic lupus erythematosus (SLE). Analysis of CD4+ T cells from individuals with SLE now shows that type I interferon intervenes with the transcriptional regulators AHR and JUN to downregulate expression of IL-22, which promotes tissue regeneration, and upregulate the expression of CXCL13, which supports lymphoid structure formation.\",\"PeriodicalId\":18810,\"journal\":{\"name\":\"Nature Reviews Rheumatology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":29.4000,\"publicationDate\":\"2024-09-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Reviews Rheumatology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41584-024-01164-y\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Reviews Rheumatology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41584-024-01164-y","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
I型干扰素在系统性红斑狼疮（SLE）的免疫发病机制中起着至关重要的作用。对来自系统性红斑狼疮患者的 CD4+ T 细胞的分析表明，I 型干扰素与转录调节因子 AHR 和 JUN 相互干预，下调促进组织再生的 IL-22 的表达，上调支持淋巴结构形成的 CXCL13 的表达。
Interferon disrupts immune and tissue homeostasis in SLE via CXCL13
Type I interferon has a crucial role in the immunopathogenesis of systemic lupus erythematosus (SLE). Analysis of CD4+ T cells from individuals with SLE now shows that type I interferon intervenes with the transcriptional regulators AHR and JUN to downregulate expression of IL-22, which promotes tissue regeneration, and upregulate the expression of CXCL13, which supports lymphoid structure formation.
期刊介绍：
Nature Reviews Rheumatology is part of the Nature Reviews portfolio of journals. The journal scope covers the entire spectrum of rheumatology research. We ensure that our articles are accessible to the widest possible audience.
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