{"title":"肌萎缩侧索硬化症患者神经胶质细胞被撕裂","authors":"Alexis M. Johnson, John R. Lukens","doi":"10.1016/j.immuni.2025.03.013","DOIUrl":null,"url":null,"abstract":"While neuroinflammatory responses driven by microglia and astrocytes have been extensively linked to neurodegenerative disease progression in amyotrophic lateral sclerosis (ALS), the specific pathways that coordinate glial cell-dependent neuroinflammation in ALS remain poorly defined. In this issue of <em>Immunity</em>, Zelic et al.<span><span><sup>1</sup></span></span> identified RIPK1 as a pivotal regulator of glial cell-driven neuroinflammation in multiple ALS models.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"92 1","pages":""},"PeriodicalIF":25.5000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Glia get RIPped in ALS\",\"authors\":\"Alexis M. Johnson, John R. Lukens\",\"doi\":\"10.1016/j.immuni.2025.03.013\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"While neuroinflammatory responses driven by microglia and astrocytes have been extensively linked to neurodegenerative disease progression in amyotrophic lateral sclerosis (ALS), the specific pathways that coordinate glial cell-dependent neuroinflammation in ALS remain poorly defined. In this issue of <em>Immunity</em>, Zelic et al.<span><span><sup>1</sup></span></span> identified RIPK1 as a pivotal regulator of glial cell-driven neuroinflammation in multiple ALS models.\",\"PeriodicalId\":13269,\"journal\":{\"name\":\"Immunity\",\"volume\":\"92 1\",\"pages\":\"\"},\"PeriodicalIF\":25.5000,\"publicationDate\":\"2025-04-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Immunity\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.immuni.2025.03.013\",\"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":"Immunity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.immuni.2025.03.013","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
虽然小胶质细胞和星形胶质细胞驱动的神经炎症反应与肌萎缩性脊髓侧索硬化症(ALS)中神经退行性疾病的进展有着广泛的联系,但协调 ALS 中神经胶质细胞依赖性神经炎症的特定通路仍未明确。在本期《免疫》杂志上,Zelic 等人1 发现 RIPK1 是多种 ALS 模型中神经胶质细胞驱动的神经炎症的关键调节因子。
While neuroinflammatory responses driven by microglia and astrocytes have been extensively linked to neurodegenerative disease progression in amyotrophic lateral sclerosis (ALS), the specific pathways that coordinate glial cell-dependent neuroinflammation in ALS remain poorly defined. In this issue of Immunity, Zelic et al.1 identified RIPK1 as a pivotal regulator of glial cell-driven neuroinflammation in multiple ALS models.
期刊介绍:
Immunity is a publication that focuses on publishing significant advancements in research related to immunology. We encourage the submission of studies that offer groundbreaking immunological discoveries, whether at the molecular, cellular, or whole organism level. Topics of interest encompass a wide range, such as cancer, infectious diseases, neuroimmunology, autoimmune diseases, allergies, mucosal immunity, metabolic diseases, and homeostasis.