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被设计成表达细胞外囊内化受体的树突细胞原始细胞增强了小鼠模型中的癌症免疫疗法

Ali Ghasemi^1,2,3, Amaia Martinez-Usatorre^1,2,3, Yang Liu^1,2,3

¹Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, Swiss Federal Institute of Technology in Lausanne (EPFL), Lausanne, Switzerland.

Nature communications

|October 15, 2025

概括

工程造型的树突细胞原始体 (DCPs) 表达IL-12和细胞外囊内化受体 (EVIR) 增强癌症免疫疗法. 这种新的方法在黑色素瘤模型中改善了T细胞参与和PD-1阻断功效.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
生物技术是生物技术.

背景情况:

用树突细胞 (DC) 进行的癌症免疫疗法显示出适度的临床疗效.
现有的方法需要活体抗原脉冲,限制了更广泛的应用.
瘤抗原损失是免疫疗法耐药性的关键机制.

研究的目的:

为增强癌症免疫疗法设计树突细胞原始细胞 (DCPs).
通过细胞外囊 (EVs) 开发一种用于DC与瘤抗原交叉穿衣的新方法.
为了提高癌症免疫疗法的疗效,包括PD-1阻断,在耐药黑色素瘤模型中.

主要方法:

DCPs被设计为表达IL-12和细胞外囊内化受体 (EVIR).
EVIR在癌细胞及其EV上与GD2 disialoganglioside结合,从而促进cDC1的EV内部化.
工程 DCPs 系统地给小鼠,并评估它们对瘤免疫力的影响.

主要成果:

工程 DCPs 显示轻度,暂时的肝酶升高,并获得瘤衍生的材料.
DCPs促进了cDC1与瘤抗原的交叉结合,增强了T细胞的参与.
在免疫疗法耐药黑色素瘤模型中观察到PD-1阻断疗效的显著改善.

结论:

EVIR设计的DCP为癌症免疫疗法提供了一个有前途的策略,没有ex vivo抗原脉冲.
这种方法可以克服抗原逃逸机制,这是当前免疫疗法的关键局限性.
工程 DCP 增强抗瘤 T 细胞反应,并提高检查点阻塞疗法的疗效.

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