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在NSCLC中,HMGB1抑制IFN-γ诱导的PD-L1表达

Shumin Wang¹, Feng Li¹, Liubo Zhang¹

¹Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P. R. China.

Journal of immunology (Baltimore, Md. : 1950)

|June 28, 2025

概括

高流动性组蛋白B1 (HMGB1) 抑制非小细胞肺癌中的PD-L1表达,增强T细胞抗瘤活性. 在肺癌中,HMGB1作为嵌合式抗原受体T细胞治疗的预后指标.

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:

瘤细胞对抗瘤免疫非常重要,它们释放诸如干扰素- (IFN-γ) 等细胞因子,以消除瘤细胞.
IFN-γ可以诱导瘤细胞上的PD-L1表达,从而通过PD-1结合抑制T细胞功能.
高流动性组蛋白B1 (HMGB1) 可以增强T细胞活性和细胞因子分泌,但其在非小细胞肺癌 (NSCLC) 中PD-L1表达中的作用尚不清楚.

研究的目的:

研究HMGB1对NSCLC中PD-L1表达的影响.
在NSCLC患者中确定HMGB1,PD-L1和IFN-γ之间的相关性.
阐明HMGB1影响PD-L1表达和T细胞介导的抗瘤反应的机制.

主要方法:

在NSCLC瘤组织中分析HMGB1和PD-L1表达和癌症基因组图谱 (TCGA) 数据.
在体外实验中使用HMGB1,RAGE (高级糖化最终产品的受体),IFN-γ和NSCLC细胞系.
对JAK1/STAT3信号通路的研究.
在体外和体内评估HMGB1对仿真抗原受体 (CAR) T细胞抗瘤活性和瘤生长的影响.

主要成果:

在高IFN-γ水平的NSCLC患者中观察到HMGB1和PD-L1表达之间存在负相关性,TCGA数据证实了这一点.
HMGB1与RAGE结合,并通过抑制JAK1/STAT3通路来抑制IFN-γ诱导的PD-L1表达.
HMGB1增强了CAR T细胞的抗瘤功效,并在体外和体内抑制了瘤生长.

结论:

在NSCLC中,HMGB1抑制IFN-γ诱导的PD-L1表达,从而增强T细胞介导的抗瘤作用.
在接受CAR T细胞治疗的肺癌患者中,HMGB1显示出作为预后生物标志物的潜力.

关键词:

CD8+ T 细胞 CD8+ T 细胞高流动性组蛋白B1的蛋白质编程细胞死亡连接体 1 编程细胞死亡连接体

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