ARID1A 在 STING 中的 "循环 "缺失。

IF 13.1 1区医学 Q1 IMMUNOLOGY

Trends in Immunology Pub Date : 2024-08-01 Epub Date: 2024-07-25 DOI:10.1016/j.it.2024.07.001

Sangeeta Goswami, Padmanee Sharma

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引用次数: 0

摘要

Maxwell等人在最近的一篇文章中报告说，染色质重塑SWI/SNF复合物的一个组成部分--肿瘤细胞特异性富AT相互作用结构域1A（ARID1A）的缺失通过R-环介导的I型干扰素（IFN）通路上调触发抗肿瘤免疫。这些最新发现揭示了携带 ARID1A 功能缺失突变的患者对免疫检查点疗法（ICT）的反应有所改善的分子机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Loss of ARID1A 'loops' in STING.

In a recent article, Maxwell et al. report that loss of tumor cell-specific AT-rich interaction domain 1A (ARID1A), a component of the chromatin remodeling SWI/SNF complex, triggers antitumor immunity via R-loop-mediated upregulation of the type-I interferon (IFN) pathway. These recent findings uncover a molecular mechanism underlying improved responses to immune checkpoint therapy (ICT) seen in patients harboring an ARID1A loss-of-function mutation.

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来源期刊

Trends in Immunology 医学-免疫学

CiteScore

25.10

自引率

0.60%

发文量

130

审稿时长

6-12 weeks

期刊介绍： Trends in Immunology serves as a vital platform for tracking advancements across various areas of immunology, offering concise reviews and hypothesis-driven viewpoints in each issue. With additional sections providing comprehensive coverage, the journal offers a holistic view of immunology. This broad perspective makes it an invaluable resource for researchers, educators, and students, facilitating the connection between basic and clinical immunology. Recognized as one of the top monthly review journals in its field, Trends in Immunology is highly regarded by the scientific community.