破坏CD38驱动的T细胞功能障碍恢复了对癌症免疫疗法的敏感性
Or-Yam Revach1,2,3, Angelina M Cicerchia1, Ofir Shorer4
1Mass General Cancer Center, Krantz Family Center for Cancer Research, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
bioRxiv : the preprint server for biology
|February 26, 2024
概括
向与T细胞枯竭相关的酶CD38可以克服对癌症免疫疗法的抵抗力. 阻断CD38恢复T细胞功能,并增强对黑色素瘤免疫检查点阻断的反应.
科学领域:
- 免疫学 免疫学 免疫学
- 癌症生物学 癌症生物学
- 代谢途径 代谢途径
背景情况:
- 免疫检查点阻塞 (ICB) 治疗在大约50%的转移性黑色素瘤患者中受到抵抗的限制.
- 由瘤微环境驱动的T细胞耗尽是ICB抗性的关键机制.
- CD38是一种降解尼古丁胺氨酸二核酸 (NAD+) 的酶,与T细胞功能障碍有关.
结论:
- CD38-NAD+轴在促进T细胞耗尽和ICB抵抗方面发挥着至关重要的作用.
- 向CD38代表了一种有希望的治疗策略,以提高癌症免疫疗法的疗效.
- 从临床上讲,来自患者的3D瘤模型证明了CD38导向疗法的潜力.
关键词:
3D微流体培养方法CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38 CD38它们是NAD+NAD+NAD.在PD-1中使用PD-1.T细胞耗尽的情况.细胞因子 细胞因子免疫疗法 免疫疗法器官类型的瘤球形状物更多相关视频
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