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首页> 外文期刊>Cancer Cell >Clonally Expanded T Cells Reveal Immunogenicity of Rhabdoid Tumors
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Clonally Expanded T Cells Reveal Immunogenicity of Rhabdoid Tumors

机译：克隆扩增的T细胞揭示了rhabdoid肿瘤的免疫原性

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Rhabdoid tumors (RTs) are genomically simple pediatric cancers driven by the biallelic inactivation of SMARCB1, leading to SWI/SNF chromatin remodeler complex deficiency. Comprehensive evaluation of the immune infiltrates of human and mice RTs, including immunohistochemistry, bulk RNA sequencing and DNA methylation profiling studies showed a high rate of tumors infiltrated by T and myeloid cells. Single-cell RNA (scRNA) and T cell receptor sequencing highlighted the heterogeneity of these cells and revealed therapeutically targetable exhausted effector and clonally expanded tissue resident memory CD8(+) T subpopulations, likely representing tumor-specific cells. Checkpoint blockade therapy in an experimental RT model induced the regression of established tumors and durable immune responses. Finally, we show that one mechanism mediating RTs immunogenicity involves SMARCB1-dependent re-expression of endogenous retroviruses and interferon-signaling activation.
机译：横纹肌样肿瘤（RTs）是由SMARCB1双等位基因失活导致的基因组简单的儿童癌症，导致SWI/SNF染色质重塑复合物缺陷。对人类和小鼠RTs免疫浸润的综合评估，包括免疫组织化学、批量RNA测序和DNA甲基化分析研究表明，T细胞和髓样细胞浸润的肿瘤发生率很高。单细胞RNA（scRNA）和T细胞受体测序强调了这些细胞的异质性，并揭示了治疗靶向的耗尽效应子和克隆性扩增的组织驻留记忆CD8（+）T亚群，可能代表肿瘤特异性细胞。在一个实验性RT模型中，检查点阻断疗法诱导已建立肿瘤的消退和持久的免疫反应。最后，我们表明，一种介导RTs免疫原性的机制涉及内源性逆转录病毒的SMARCB1依赖性再表达和干扰素信号激活。

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