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在体外模型模仿瘤内皮细胞介导的免疫细胞重编程在肺腺癌

Morgane Krejbich¹, Emilie Navarro¹, Judith Fresquet¹

¹INSERM UMR 1307, CNRS UMR 6075, Nantes Université, Université d'Angers, Nantes, F-44000, France.

Journal of experimental & clinical cancer research : CR

|November 28, 2025

概括

非小细胞肺癌 (NSCLC) 的瘤内皮细胞 (TEC) 通过改变免疫细胞群来促进免疫抑制. 准TEC可以提高癌症免疫疗法的疗效.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
细胞生物学细胞生物学

背景情况:

瘤内皮细胞 (TEC) 是瘤微环境 (TME) 免疫反应的关键调节者.
非小细胞肺癌 (NSCLC) 中TEC介导免疫调节的机制尚未完全理解.

研究的目的:

研究NSCLC细胞如何将正常内皮细胞 (NEC) 转化为TEC.
阐明TECs对免疫细胞群和NSCLC中TME调节的影响.

主要方法:

在2D和3D模型中与NSCLC细胞系共同培养NEC.
对TEC的转录组,蛋白组和基因组分析.
3D多细胞瘤球体 (MCTS) 的单细胞RNA测序.

主要成果:

NSCLC共同培养诱导了TECs的显著转录和蛋白质变化,包括促炎途径变化.
TECs表现出下调的OX40L,受损的CD8+T细胞支持,并促进了CD4+T细胞偏向到Treg和Th22子集.
在MCTS和患者样本中,TECs支持M2类巨分化,并且在MCTS和患者样本中发现了具有未折叠蛋白质反应特征的明显炎症TEC亚群.
在MCTS中发现了通过MIF信号与TEC相互作用的周周M2类巨细胞子集.

结论:

在NSCLC中的TEC通过促进免疫抑制来积极重塑TME.
TECs表现出复杂的免疫调节功能,影响各种免疫细胞类型.
研究结果表明,TEC和相关的信号通路是改善NSCLC免疫疗法的潜在治疗点.

关键词:

三维模型是3D模型.在 CAF 中,CAF 是 CAF.与癌症相关的纤维细胞细胞.豁免权是一种豁免权.巨细胞是一个巨细胞.在NSCLCLC中,我们可以看到.这就是ScRNA-seqq.球形球形是指一个球形状的球体.瘤内皮细胞是瘤内皮细胞.瘤微环境是一个微环境.

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