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对CAR-T细胞进行表观遗传重编程,使其在体内对固体瘤具有功能性持续性

Michael Saitakis¹

¹Mnemo Therapeutics, 101 Boulevard Murat, 75016, Paris, France. michael.saitakis@mnemo-tx.com.

Genes and immunity

|February 22, 2024

概括

在CAR T细胞中破坏SUV39H1可增强它们在固体瘤中的持久性和抗瘤功能. 这种遗传重编程产生了自我更新的,类似干细胞的T细胞,提高了采用细胞治疗的疗效.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

卡尔T细胞疗法面临的挑战是有限的扩张和固体瘤的持久性,阻碍了治疗的有效性.
SUV39H1,一个组分离子甲基转移酶,促进异染色素的形成,这可以抑制T细胞的功能.

研究的目的:

调查SUV39H1遗传破坏对CAR T细胞功能和固体瘤中的持久性影响.
探索SUV39H1无活化的潜力,以增强采用细胞疗法.

主要方法:

在人类CAR T细胞中SUV39H1的遗传破坏.
单细胞转录组 (scRNA-seq) 和染色体可访问性 (scATAC-seq) 分析.
在瘤复发的临床前模型中评估CAR T细胞功能和持久性.

主要成果:

SUV39H1的破坏导致CAR T细胞重编程成为自我更新的干细胞样群体.
改造的CAR T细胞表现出功能障碍基因的表达减少.
由于SUV39H1的不活化,在多次瘤复发时产生了强大而持久的抗瘤功能.

结论:

无活化SUV39H1是一种可行的策略,可以增强CAR T细胞在固体瘤中的功能持久性和抗瘤活性.
这种方法为改善固体癌症患者的采用细胞疗法提供了一种安全有效的方法.

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