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防范未经控制的BATF3诱导的CAR T细胞扩张

Nayan Jain^1,2, Zeguo Zhao², Judith Feucht^2,3

¹Louis V. Gerstner Jr Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Centre, New York, NY, USA.

|February 9, 2023

概括

在仿真抗原受体 (CAR) T 细胞中破坏TET2基因可增强瘤排斥,但有危险的,不受控制的细胞生长风险. 在CAR T细胞疗法中,TET2作为防范这种增殖的守护者,防止基因组不稳定.

科学领域:

免疫学
细胞生物学
癌症治疗

背景情况:

化学抗原受体 (CAR) T 细胞治疗的疗效需要进一步提高.
表观遗传特征影响T细胞的分化和功能.
表观遗传调节器十-十一转位2 (TET2) 是增强T细胞功能的潜在目标.

研究的目的:

研究TET2在CAR T细胞的性能和安全性的作用.
探索表观遗传编程作为改善CAR T细胞疗法的策略.
了解TET2对T细胞增殖和功能影响的机制.

主要方法:

在T细胞中破坏TET2基因.
在白血病和前列腺癌模型中评估T细胞介导的瘤排斥.
对CAR T细胞的克隆扩张,基因表达 (BATF3,MYC) 和基因组稳定性的分析.

主要成果:

在临床前模型中,TET2干扰增强了T细胞介导的瘤排斥.
TET2的丧失促进了抗原独立的CAR T细胞的克隆扩张和组织透.
这种依赖于双基因TET2和BATF3损失的增殖导致效应器功能降低和基因组不稳定性增加.
作为一个关键的调节剂,TET2 防止异常的 CAR T 细胞增殖和相关风险.

结论:

通过TET2向的表观遗传编程显示了增强T细胞免疫力的潜力.
干扰TET2具有不受控制的CAR T细胞增殖和基因组不稳定性的重大风险.
在CAR T细胞疗法中,TET2对于维持T细胞平衡和防止瘤转化至关重要.

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