用 TL1A 敲响肺部的警钟。

IF 12.6 1区 医学 Q1 IMMUNOLOGY
Journal of Experimental Medicine Pub Date : 2024-06-03 Epub Date: 2024-04-10 DOI:10.1084/jem.20240389
Silvia Pires, Randy S Longman
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引用次数: 0

摘要

环境空气中的抗原是过敏性哮喘发病的核心因素,但引发疾病的细胞过程仍不完全清楚。在这份报告中,Schmitt 等人(https://doi.org/10.1084/jem.20231236)发现 TNF 样蛋白 1A(TL1A)是由肺上皮细胞亚群组成性表达的上皮警戒素,它会在空气传播的微生物挑战时释放,并与 IL-33 协同驱动过敏性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sounding the alarm in the lung with TL1A.

Environmental airborne antigens are central to the development of allergic asthma, but the cellular processes that trigger disease remain incompletely understood. In this report, Schmitt et al. (https://doi.org/10.1084/jem.20231236) identify TNF-like protein 1A (TL1A) as an epithelial alarmin constitutively expressed by a subset of lung epithelial cells, which is released in response to airborne microbial challenge and synergizes with IL-33 to drive allergic disease.

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来源期刊
CiteScore
26.60
自引率
1.30%
发文量
189
审稿时长
3-8 weeks
期刊介绍: Since its establishment in 1896, the Journal of Experimental Medicine (JEM) has steadfastly pursued the publication of enduring and exceptional studies in medical biology. In an era where numerous publishing groups are introducing specialized journals, we recognize the importance of offering a distinguished platform for studies that seamlessly integrate various disciplines within the pathogenesis field. Our unique editorial system, driven by a commitment to exceptional author service, involves two collaborative groups of editors: professional editors with robust scientific backgrounds and full-time practicing scientists. Each paper undergoes evaluation by at least one editor from both groups before external review. Weekly editorial meetings facilitate comprehensive discussions on papers, incorporating external referee comments, and ensure swift decisions without unnecessary demands for extensive revisions. Encompassing human studies and diverse in vivo experimental models of human disease, our focus within medical biology spans genetics, inflammation, immunity, infectious disease, cancer, vascular biology, metabolic disorders, neuroscience, and stem cell biology. We eagerly welcome reports ranging from atomic-level analyses to clinical interventions that unveil new mechanistic insights.
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