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宿主衍生的互白素-1α通过重编程与瘤相关的髓质细胞来驱动瘤免疫抑制

Manikanda Raja Keerthi Raja^1,2, Gourab Gupta¹, Grace Atkinson¹

¹Department of Biological Sciences, University of South Carolina, Columbia, SC, USA.

NPJ breast cancer

|January 17, 2026

概括

干白素-1α (IL-1α) 驱动乳腺癌中的免疫抑制性瘤微环境 (TME). 阻断IL-1α增强了抗瘤免疫力,并提出了一个潜在的治疗策略.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
癌症生物学癌症生物学

背景情况:

骨髓状细胞创造了一个免疫抑制瘤微环境 (TME).
在TME中控制髓状细胞分化的机制尚未完全理解.
介素-1α (IL-1α) 在TME内的髓状细胞分化中的作用需要研究.

研究的目的:

调查IL-1α在骨髓细胞分化和乳腺癌中TME调节中的作用.
确定乳腺癌中由IL-1α调节的细胞源和信号通路.

主要方法:

采用了Orthotopic小鼠乳腺癌模型.
单细胞RNA测序 (scRNA-seq) 在瘤透髓状细胞上进行.
用CellChat分析来研究细胞间通信.
在实验室中对来自骨的巨细胞进行了分化.

主要成果:

主体介质素-1α (IL-1α) 的删除导致了瘤的完全排斥.
鉴定出CX3CR1+巨细胞是TME中IL-1α的主要来源.
缺少IL-1α改变了单细胞-巨细胞分化,减少了CX3CR1+巨细胞,增加了iNOS+巨细胞.
来自IL-1α缺乏宿主的髓状细胞减少了CD8+ T细胞上的PD-1和CTLA-4表达.
失去IL-1α重新编程了免疫细胞的通信,影响了M-CSF,TGFβ和PGE2信号通路.
前列腺素E2 (PGE2) 逆转了IL-1α缺陷巨细胞中的亲炎性表型.

结论:

IL-1α在乳腺癌中促进免疫抑制性TME,部分通过PGE2信号传递.
阻断IL-1α代表了乳腺癌的潜在治疗策略.
了解IL-1α在髓状细胞分化中的作用对于癌症免疫治疗至关重要.

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