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口腔状细胞癌驱动单细胞进入免疫抑制的CD25⁺CD163⁺CD206⁺巨细胞

Hector F Pelaez-Prestel¹, Fernando Gonzalez-Martin¹, Alvaro Ras-Carmona¹

¹Department of Immunology, Ophthalmology and ORL, School of Medicine, Complutense University of Madrid, Pza Ramon y Cajal, s/n, 28040 Madrid, Spain.

|October 22, 2024

概括

口腔状细胞癌细胞介质驱动单细胞分化成免疫抑制M2巨细胞. 这些巨细胞抑制T细胞反应,为瘤微环境做出贡献,并支持口腔癌的生长.

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:

瘤相关巨细胞 (TAMs) 是口腔状细胞癌 (OSCC) 瘤微环境中的关键参与者.
TAMs通常源于循环的单细胞在瘤内分化.
了解TAM分化对于开发有效的癌症疗法至关重要.

研究的目的:

研究口腔癌细胞系如何影响单细胞分化.
从暴露于OSCC细胞培养基 (CM) 的单细胞中获得的巨细胞的表型和功能进行表征.
识别OSCCCM内负责诱导特定巨细胞表型的因素.

主要方法:

单细胞与来自OSCC细胞系 (H413,TR146) 的CM进行培养.
通过表达表面标记物 (CD163,CD206,CD11c,CD86,HLA-DR) 来评估巨细胞分化.
进行了T细胞激活测定,CM的蛋白质组分析和分化巨细胞的RNA测序.

主要成果:

在OSCC CM中诱导单细胞分化成M2类巨细胞 (CD163+,CD206+).
这些M2巨细胞抑制了T细胞的激活和增殖.
在CM中溶解的蛋白质,可能包括补充因子H和等离子体激活剂抑制剂1,介导了这种差异化.
转录组分析显示了免疫抑制特征,包括增加IL2RA (CD25) 表达.

结论:

OSCC细胞系分泌的因素促进免疫抑制TAMs从单细胞的发展.
这一过程有助于OSCC中的免疫抑制瘤微环境.
这些发现提供了对OSCC病原体和潜在治疗点的见解.

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