Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri.
Cancer Discov. 2024 Feb 8;14(2):208-210. doi: 10.1158/2159-8290.CD-23-1361.
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) .
MHC-I 下调与 PDAC 的免疫治疗抵抗相关，但提高细胞表面 MHC-I 的有效策略仍很缺乏。这项由 Sang、Zhou、Chen、Yu 及其同事进行的研究发现，抑制肿瘤内固有 RIPK2 可作为一种药理学靶点，阻止肿瘤细胞上 MHC-I 的降解，并改善 PDAC 对抗 PD-1 免疫治疗的反应。见 Sang 等人的相关文章，第 326 页(1)。
