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在转移性乳腺癌中,p38阻塞逆转了免疫抑制瘤微环境

Priyanka Rajan¹, Robert Zollo¹, Yanqi Guo¹

¹Roswell Park Comprehensive Cancer Center.

Research square

|November 24, 2025

概括

阻断p38α通过增强CD8+T细胞活性和减少免疫抑制性髓状细胞来减少乳腺癌的转移. 这揭示了改善抗瘤免疫力的新治疗标.

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:

转移性乳腺癌 (MBC) 由于免疫抑制性瘤微环境 (TME),具有有限的治疗选择.
TME阻碍了有效的抗瘤免疫反应,促进了癌症的进展和转移.

研究的目的:

调查p38α作为TME中的可药物标.
阐明p38α在调节免疫-瘤相互作用和转移中的作用.

主要方法:

系统性阻断p38α,CD8+ T细胞枯竭,CRISPR/Cas9介导的p38α失活.
单细胞转录组分析,免疫类型定型,体外增殖试验.

主要成果:

p38α阻断减少了转移,取决于CD8+ T细胞.
抑制p38α逆转了CD8+T细胞的耗尽,增强了它们的激活,并减少了抑制受体 (PD-1,LAG-3,CTLA-4).
p38α阻塞影响了髓状细胞群 (MDSC,TAM) 和减少了亲髓状细胞因子/化学因子和外体.

结论:

p38α是免疫抑制性TME和乳腺癌转移的关键驱动因素.
治疗阻断p38α通过调节T细胞和髓状细胞来增强抗瘤免疫力,从而有可能改善患者的治疗结果.

关键词:

免疫抑制免疫抑制转移性乳腺癌转移性乳腺癌来自骨髓细胞的抑制细胞.在p38中,p38是什么?单细胞RNA测序的一个单细胞RNA测序.瘤微环境是一个微环境.与瘤相关的巨细胞.

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