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DDR2/STAT3正反循环通过调节PD-L1和招募oxaliplatin耐药HCC中的MDSC来调解免疫抑制的微环境

Wenfeng Liu¹, Feng Zhang², Bing Quan²

¹Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Interventional Medicine, Shanghai, China; Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai, China.

Cellular and molecular gastroenterology and hepatology

|July 5, 2024

概括

一个DDR2和STAT3的反循环通过促进免疫逃逸,驱动肝癌中牛氧的耐药性. 针对这种途径可以克服肝细胞癌 (HCC) 中的化学抵抗和免疫逃逸.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

高度的DDR2表达在抗氧沙的肝细胞癌 (HCC) 中被观察到.
在HCC中,DDR2在抗氧化抗性和免疫逃避中发挥作用.

研究的目的:

研究DDR2在HCC中抗氧化抗性的作用.
探索DDR2介导的免疫逃避在HCC中的机制.

主要方法:

已确立的抗氧沙的HCC细胞系.
研究了DDR2和STAT3相互作用以及DDR2/STAT3介导的PD-L1上调和PMN-MDSC积累在体外和体内.
分析了DDR2/STAT3反循环,PD-L1和CCL20转录,以及PD-L1抗体和CCL20阻塞的治疗作用.

主要成果:

在抗氧化抗性HCC中发现了一个DDR2/STAT3正反循环,促进PD-L1上调和PMN-MDSC积累.
对DDR2/STAT3敏感细胞对氧化,减少PMN-MDSC和增加CD8+T细胞的敲除.
HCC细胞通过CCL20招募PMN-MDSC,STAT3直接增强PD-L1和CCL20的转录.

结论:

DDR2/STAT3通路调解一个免疫抑制的微环境,促进氧沙抗性和免疫逃避.
针对DDR2/STAT3途径为HCC化学抵抗和免疫逃逸提供了潜在的治疗策略.

关键词:

这就是DDR2 DDR2.肝细胞癌肝细胞癌在MDSCs中.PD-L1 升级调节的方法在STAT3中,我们可以使用STAT3.

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