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CD25高效能调节T细胞阻碍对三阴性乳腺癌中PD-1阻断的反应

Stéphane Fattori^1,2, Aude Le Roy³, Jemila Houacine³

¹Team Immunity and Cancer, Centre de Recherche en Cancérologie de Marseille (CRCM), Inserm, U1068, CNRS, UMR7258, Institut Paoli-Calmettes, Aix-Marseille University, UM105, Marseille, France.

Cancer research

|June 28, 2023

概括

调控性T细胞 (Tregs) 阻碍了三阴性乳腺癌 (TNBC) 的抗瘤免疫力. 针对CD25+效应因子Tregs与PD-1阻断一起,可以恢复免疫反应并改善TNBC患者的治疗结果.

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:

众所周知,调节性T细胞 (Tregs) 抑制抗瘤免疫力.
在三阴性乳腺癌 (TNBC) 临床结果中Tregs的特定作用尚未完全理解.
在TNBC中,免疫抑制的微环境的特征是效应体CD8+T细胞和高度抑制效应体Tregs (eTregs) 之间的不平衡.

研究的目的:

调查效应体Tregs (eTregs) 在PD-1阻塞抗性TNBC中的作用.
在TNBC中识别eTreg耗尽的选择性标记.
评估结合抗CD25治疗与TNBC中PD-1阻断的治疗潜力.

主要方法:

对抗PD-1封锁的TNBC患者瘤内ETregs的分析.
在初级和转移性TNBC中确定eTregs的选择性表面标记物.
在同源性TNBC模型中,对抗CD25抗体与PD-1阻断结合的评估.

主要成果:

内eTregs表达高水平的PD-1并且存在于PD-1阻塞抵抗性TNBC中.
CD25被确定为TNBC中eTregs最有选择性的表面标记物.
在TNBC模型中,用抗CD25抗体和PD-1阻断的联合治疗增强了全身抗瘤免疫力,并控制了瘤生长.

结论:

有利于eTregs而不是效应细胞CD8+T细胞的不平衡导致了PD-1阻塞耐药TNBC中的免疫抑制微环境.
在TNBC中,CD25是消耗eTregs的一个有希望的目标.
将抗CD25疗法与PD-1阻断相结合提供了一种潜在的策略,以克服耐药性并提高TNBC的治疗疗效.

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