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核酸受体P2X7/STAT6通路调节巨细胞M2极化及其在CAR-T免疫治疗中的应用

Qin Si¹, Lu Yang², Jie Liu³

¹the Inner Mongolia Key Laboratory for Molecular Regulation of the Cell and the State Key Laboratory of Reproductive Regulation, School of Life Sciences, Inner Mongolia University, Hohhot 010010, Inner Mongolia Autonomous Region, P.R. China.

|December 18, 2024

概括

抑制巨细胞中的P2X7受体逆转M2极化,并增强化学抗原受体-T细胞 (CAR-T) 治疗对卵巢癌的疗效. 这种方法克服了免疫抑制性瘤微环境,增强了抗瘤活性.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
细胞生物学细胞生物学

背景情况:

卵巢癌 (OC) 化学抗原受体-T细胞 (CAR-T) 治疗通常由于免疫抑制瘤微环境而失败.
瘤透的M2极化巨细胞有助于这种免疫抑制.
P2X7受体在M2巨细胞中表达,并与它们的两极分化有关.

研究的目的:

研究是否沉默巨细胞中的P2X7受体可以增强卵巢癌中CAR-T细胞的抗瘤功效.
探索P2X7受体和STAT6在巨细胞极化和CAR-T细胞功能中的作用.

主要方法:

在实验室中分化了巨细胞,P2X7受体被静止,有或没有STAT6过度表达.
使用流细胞计,ELISA和qRT-PCR评估了巨细胞极化标记 (M1/M2).
针对非功能性P2X7 (nfP2X7) 的CAR-T细胞与修饰的巨细胞和OC细胞共同培养,以评估抗瘤作用.

主要成果:

P2X7受体沉默促进了M1标记物 (CD86,TNF-α,IL-6,IL-1β) 和减少了M2标记物 (CD206,IL-10),抑制了STAT6酸化.
STAT6过度表达逆转了这些影响.
M2巨细胞抑制了CAR-T细胞的抗瘤活性,但P2X7受体沉默取消了这种免疫抑制.

结论:

沉默P2X7受体可以通过抑制STAT6激活来逆转M2巨分化.
这一策略在卵巢癌模型中增强了向nfP2X7受体的CAR-T细胞的抗瘤疗效.

关键词:

化学抗原受体T 化学抗原受体T 在M2巨细胞中.卵巢癌是发生在卵巢中的癌症.这是一个P2X7受体.在STAT6中,

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