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准骨髓层Trem2重编程免疫抑制,并在NASH驱动的肝癌发生中增强检查点免疫疗法

Ziyi Wang¹, Yu Zhang², Xiangdong Li³

¹The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.

Cancer immunology research

|August 1, 2025

概括

向巨细胞中的Trem2可以改善肝癌的免疫疗法. 阻断Trem2可降低非酒精性脂肪肝驱动性肝癌的免疫抑制,提高抗PD1疗法的有效性.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
在瘤学瘤学.

背景情况:

非酒精性脂肪肝炎 (NASH) 进展为肝细胞癌 (HCC) 与表达Trem2的巨有关.
针对NASH驱动的HCC的抗PD1免疫疗法有效性有限.

研究的目的:

研究巨细胞中的Trem2如何影响NASH驱动的HCC对免疫疗法的反应.
探索Trem2在瘤微环境中的作用及其对T细胞调节的影响.

主要方法:

对NASH患者Trem2表达的临床分析.
在小鼠模型中,Trem2 (Trem2Δmye) 的骨髓细胞特异性淘汰.
评估巨细胞重编程,NET降解和T细胞分化.
单独和与CXCR2抑制结合的抗PD1疗法疗效的评估.

主要成果:

升高的Trem2与中性粒细胞外细胞陷 (NETs) 和NASH中的特定T细胞种群相关.
骨髓细胞中Trem2的删除会损害巨细胞的重编程,并增强NET的降解.
Trem2 除抑制了TGF-β的产生和免疫抑制T细胞的分化.
通过通过NET降解降低Treg CXCR4表达,Trem2删除可以提高抗PD1疗法的疗效.

结论:

在NASH驱动的HCC中,Trem2是免疫抑制瘤微环境的关键调节者.
针对髓状细胞重编程和NETosis提供了一种潜在的组合策略,以克服代谢性肝癌中的免疫疗法耐药性.

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