Abstract：
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.
摘要：
在最近的一篇文章中，麦克斯韦等人。报告肿瘤细胞特异性AT丰富的相互作用域1A（ARID1A）的丢失，染色质重塑SWI/SNF复合物的一个组成部分，通过R-loop介导的I型干扰素（IFN）途径的上调触发抗肿瘤免疫。这些最新发现揭示了在具有ARID1A功能丧失突变的患者中观察到的改善对免疫检查点治疗（ICT）反应的分子机制。
