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免疫检查点的基因组编辑:在癌症中通过CRISPR介导的PD-1抑制

SuleimanIbrahim Mohammad¹, A K Kareem², Asokan Vasudevan³

¹Electronic Marketing and Social Media, Economic and Administrative Sciences Zarqa University, Jordan; Research follower, INTI International University, Negeri Sembilan 71800, Malaysia.

Seminars in oncology

|November 28, 2025

概括

通过CRISPR-Cas9基因组编辑,可以禁用PD-1/PD-L1免疫检查点,以增强抗瘤T细胞反应. 临床前和早期临床研究表明,癌症免疫力和疗效得到改善,尽管广泛使用仍然存在挑战.

科学领域:

免疫学免疫学免疫学
遗传学是一个遗传学.
在瘤学瘤学.

背景情况:

瘤通过PD-1/PD-L1检查点逃避免疫监测,限制T细胞的疗效.
现有的免疫检查点阻塞疗法面临抵抗和T细胞枯竭.
通过CRISPR-Cas9基因组编辑,可以精确地破坏PD-1或PD-L1以提高抗瘤免疫力.

研究的目的:

在癌症治疗中审查CRISPR介导的PD-1/PD-L1抑制.
评估基于CRISPR的免疫疗法的临床前和临床研究.
总结机械的见解和翻译的挑战.

主要方法:

CRISPR-Cas9基因编辑以淘汰T细胞中的PD-1或瘤细胞中的PD-L1.
在临床前模型中评估T细胞增殖,细胞因子生产和细胞毒性.
评估CAR T细胞疗法,组合方法和早期临床试验.

主要成果:

活体 PD-1 淘汰会增强 T 细胞抗瘤功能和瘤清除.
编辑CRISPR可以提高CAR T细胞的持久性和抗疲劳性.
在瘤中的PD-L1淘汰会重塑微环境并增强采用疗法.
早期的临床试验表明PD-1缺乏T细胞的可行性,安全性和初步疗效.

结论:

通过CRISPR介导的PD-1/PD-L1抑制是克服癌症免疫规避的有希望的策略.
多重基因组编辑和组合疗法显示出协同作用的抗瘤效应.
需要进一步的研究,以解决临床翻译的交付挑战,非目标效应和监管方面.

关键词:

收养细胞疗法采用细胞疗法.卡特细胞 CAR-T 细胞克里斯普尔-Cas9是什么意思癌症免疫疗法癌症免疫疗法在PD-1/PD-L1中.T细胞耗尽的情况.

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