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单细胞转录基因分析显示,巨细胞诱导的血管生成有助于肝细胞癌的免疫疗法抵抗

Xinyu Pan¹, Baolin Liao^2,3, Zhijie Hu^2,3

¹Key Laboratory of Gene Engineering of the Ministry of Education, Department of Biochemistry, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China.

|January 10, 2026

概括

研究人员确定了一种特定的巨细胞子集,NFKBIZ+ M0,与肝细胞癌中PD-1/PD-L1免疫治疗的耐药性有关. 这些巨细胞促进瘤生长和免疫抑制,为改善治疗疗效提供了潜在的点.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

肝细胞癌 (HCC) 是全球癌症死亡的主要原因.
瘤微环境 (TME) 显著影响HCC治疗结果,特别是免疫疗法反应.
抵抗PD-1/PD-L1阻塞,这是一个关键的免疫疗法策略,仍然是HCC的主要临床挑战.

研究的目的:

为了确定细胞机制背后的抵抗PD-1/PD-L1阻塞在HCC.
描述与免疫疗法不响应相关的新型巨细胞群.
阐明驱动免疫抑制性TME在耐药HCC中的分子途径.

主要方法:

对HCC瘤的单细胞转录组分析.
对巨细胞种群及其基因表达特征的分析.
转录监管网络分析以确定关键驱动因素.

主要成果:

在不响应抗PD-1治疗的HCC患者中发现了一种独特的NFKBIZ+ M0巨子集.
这些巨细胞表现出缺氧诱导的表型,分泌VEGFA和HBEGF促进血管生成.
这些巨细胞对CXCL2,CXCL3和CXCL8的高表达会产生免疫抑制的TME.
确定了FOSB-VEGFA和FOS-HBEGF信号通路是这种致病性表型的关键调节者.

结论:

在HCC中,NFKBIZ+巨体代表了一种新的机制,将缺氧,血管生成和免疫逃避联系起来.
这种巨细胞子集在抵抗PD-1阻塞疗法的过程中发挥了关键作用.
准NFKBIZ+巨细胞或相关途径可能提供克服HCC免疫疗法耐药性的策略.

关键词:

M0 巨细胞巨细胞肝细胞癌是肝细胞癌.免疫检查点封锁封锁转录规则转录规则转录规则瘤血管新生发生.

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