免疫检查点阻断通过扩增效应 CD8⁺ T 细胞克隆增强淋巴细胞清除性化疗诱导的抗肿瘤免疫
Immune Checkpoint Blockade Augments Lymphodepleting Chemotherapy-Induced Antitumor Immunity by Expanding Effector CD8+ T-cell Clones.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
SOX10 通过诱导 A375 黑色素瘤细胞中免疫检查点分子 PD-L1 的表达抑制 T 细胞识别
英文原题：SOX10 Inhibits T Cell Recognition by Inducing Expression of the Immune Checkpoint Molecule PD-L1 in A375 Melanoma Cells.
查看英文原题
SOX10 Inhibits T Cell Recognition by Inducing Expression of the Immune Checkpoint Molecule PD-L1 in A375 Melanoma Cells.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
研究概要
SOX10 通过表达 PD-L1，在黑色素瘤的固有免疫抑制机制中发挥作用。
中文摘要
SOX10与黑色素瘤细胞的程序及免疫逃逸相关。本研究在A375黑色素瘤细胞中通过转染和小干扰RNA（siRNA）调节SOX10表达，使用流式细胞术和蛋白质印迹检测相关分子，并通过干扰素γ（IFN-γ）ELISPOT评估NY-ESO-1特异性T细胞受体工程化T细胞（TCR-T）的反应。SOX10过表达提高了程序性死亡配体1（PD-L1）表达，并降低肿瘤细胞对TCR-T细胞攻击的易感性。结果提示SOX10可通过增强PD-L1介导的抑制，促进黑色素瘤细胞内在的免疫逃逸。
展开英文摘要原文
MATERIALS AND METHODS
SOX10 overexpression and knockdown was performed using SOX10 gene transfection and SOX10 siRNA transfection into A375 melanoma cells. PD-L1 expression was assessed by flow cytometry and western blotting. T cell response was evaluated using NY-ESO-1 specific TCR-transduced T (TCR-T) cells by IFN ELISPOT assay.
RESULTS
SOX10 overexpression increased the expression of PD-L1, whereas SOX10 knockdown, using siRNA, decreased its expression. IFN ELISPOT assay revealed that overexpression of SOX10 decreased the susceptibility of cells to NY-ESO-1-specific TCR-T cells.
CONCLUSION
SOX10 has a role in the intrinsic immune suppressive mechanisms of melanoma through expression of PD-L1.
论文信息
- 作者
- Sasaki K、Hirohashi Y、Murata K、Minowa T、Nakatsugawa M、Murai A、Mizue Y、Kubo T
- 第一作者单位
- Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.Japan
- 通讯作者单位
- Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan; torigoe@sapmed.ac.jp.Japan
- 期刊
- Anticancer research2023 Apr
- 原文标识
- PubMed 36974807 · DOI 10.21873/anticanres.16296