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放射治疗在树突细胞中诱导YTHDF2,损害交叉呈现和T细胞功能

Dapeng Chen^1,2, Liangliang Wang³, Chuangyu Wen^1,2

¹Department of Radiation and Cellular Oncology, University of Chicago, Chicago, IL, USA.

The Journal of experimental medicine

|November 6, 2025

概括

放射治疗失败和转移与树突细胞 (DCs) 中辐射诱导的免疫抑制有关. 针对DC中的YTHDF2克服了这一问题,增强了癌症治疗和疫苗.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
分子生物学分子生物学

背景情况:

转移性进展是放射治疗失败的主要原因.
连接放射治疗与免疫抑制和转移的机制尚不清楚.

研究的目的:

在树突细胞 (DC) 中识别辐射诱导的免疫检查点.
研究YTHDF2在放射治疗耐药性和转移中的作用.
探索YTHDF2向作为一种治疗策略.

主要方法:

来自临床试验的患者活检的分析 (NCT03223155).
研究了通过电离辐射对YTHDF2调节的分子机制.
在临床前模型中评估YTHDF2对T细胞激活和瘤控制的影响.

主要成果:

在放射治疗后的DC中增加YTHDF2表达与治疗失败相关.
电离辐射会诱导SPI1,而SPI1则会在DC上调节YTHDF2.
YTHDF2促进了诺奇通路调节者的降解,损害了T细胞的激活,促进了免疫逃避.
向YTHDF2恢复了DC免疫性,并增强了放射治疗的疗效.

结论:

在DC中,YTHDF2充当辐射诱导的免疫检查点.
准YTHDF2是一种有前途的策略,可以克服放射治疗耐药性和转移.
结合YTHDF2抑制和放射治疗的联合治疗可以改善癌症治疗结果和基于DC的疫苗.

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