Epstein–Barr virus (EBV) infection is an established cause of nasopharyngeal carcinoma (NPC) and is involved in a variety of malignant phenotypes, including tumor immune escape. EBV can encode a variety of circular RNAs (circRNA), however, little is known regarding the biological functions of these circRNAs in NPC. In this study, EBV-encoded circBART2.2 was found to be highly expressed in NPC where it upregulated PD-L1 expression and inhibited T-cell function in vitro and in vivo . circBART2.2 promoted transcription of PD-L1 by binding the helicase domain of RIG-I and activating transcription factors IRF3 and NF-κB, resulting in tumor immune escape. These results elucidate the biological function of circBART2.2 , explain a novel mechanism of immune escape caused by EBV infection, and provide a new immunotherapy target for treating NPC. Significance: This work demonstrates that circBART2.2 binding to RIG-I is essential for the regulation of PD-L1 and subsequent immune escape in nasopharyngeal carcinoma.

中文翻译：

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Epstein-Barr病毒编码的环状RNA CircBART2.2通过调节PD-L1促进鼻咽癌的免疫逃逸


EB 病毒 (EBV) 感染是鼻咽癌 (NPC) 的确定原因，并与多种恶性表型有关，包括肿瘤免疫逃逸。 EBV可以编码多种环状RNA（circRNA），然而，人们对这些circRNA在NPC中的生物学功能知之甚少。在这项研究中，发现 EBV 编码的 circBART2.2 在 NPC 中高表达，在体外和体内上调 PD-L1 表达并抑制 T 细胞功能。 circBART2.2通过结合RIG-I的解旋酶结构域并激活转录因子IRF3和NF-κB来促进PD-L1的转录，从而导致肿瘤免疫逃逸。这些结果阐明了circBART2.2的生物学功能，解释了EBV感染引起的免疫逃逸的新机制，为鼻咽癌的治疗提供了新的免疫治疗靶点。意义：这项工作表明，circBART2.2 与 RIG-I 的结合对于鼻咽癌中 PD-L1 的调节和随后的免疫逃逸至关重要。