Summary: MHC-I downregulation is correlated with immunotherapy resistance in PDAC, but efficient strategies to increase cell-surface MHC-I are still lacking. This study by Sang, Zhou, Chen, Yu, and colleagues identified inhibition of tumor-intrinsic RIPK2 as a pharmacologic target to block the degradation of MHC-I on tumor cells and improved PDAC responses to anti–PD-1 immunotherapy. See related article by Sang et al., p. 326 (1) .

中文翻译：

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“破解”胰腺癌对免疫监视的阻碍

摘要：MHC-I 下调与 PDAC 免疫治疗耐药相关，但仍缺乏增加细胞表面 MHC-I 的有效策略。 Sang、Zhou、Chen、Yu 及其同事的这项研究确定了抑制肿瘤内在 RIPK2 作为药理学靶点，可阻止肿瘤细胞上 MHC-I 的降解，并改善 PDAC 对抗 PD-1 免疫疗法的反应。参见 Sang 等人的相关文章，第 17 页。 326（1）。