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通过免疫检查点封锁的巨细胞再极化驱动T细胞参与瘤微环境

Tina Kwok¹, Ildefonso A Silva-Junior¹, Sara Korpe¹

¹Department of Immunology, Mayo Clinic, Phoenix, AZ 85054, USA.

|October 6, 2025

概括

组合免疫疗法通过促进瘤微环境 (TME) 内的T细胞和巨细胞相互作用来增强抗瘤反应. 针对PD-1和PD-L1都是有效控制瘤的关键.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
医学科学医学科学医学科学

背景情况:

瘤微环境 (TME) 相互作用是免疫治疗成功的关键.
与瘤相关的巨细胞 (TAMs) 在TME内的免疫反应中起着关键作用.
了解TAM在组合免疫治疗中的作用对于改善患者的治疗结果至关重要.

研究的目的:

研究联合抗编程细胞死亡蛋白1 (PD-1) 和抗编程死亡配体1 (PD-L1) 免疫疗法的协同机制.
为了阐明CD8+ T细胞和TAMs在TME内联合免疫疗法的反应中的相互作用.
探索抗PD-L1治疗引起的TAM功能变化及其对T细胞活性的影响.

主要方法:

利用一种小鼠模型进行联合抗PD-1和抗PD-L1检查点阻塞疗法.
采用活细胞成像来可视化T细胞-TAM在TME中的相互作用.
分析了免疫细胞透,TAM再极化 (M1-类) 和巨细胞功能标记物 (促炎因素,细胞活性).

主要成果:

组合免疫疗法导致CD8+ T细胞透率增加和M1-样TAM再极化.
活细胞成像显示,在组合治疗中,CD8+ T细胞和TAM接触接口的增强.
抗PD-L1治疗增加了巨细胞的促炎因素和细胞活性,表明T细胞的活性.
完整的瘤控制需要抗PD-1和抗PD-L1的组合,强调了双重向的必要性.

结论:

结合免疫疗法涉及PD-1/PD-L1阻塞重塑TME以增强抗瘤免疫力.
TAMs是调解治疗协同作用的关键参与者,而抗PD-L1促进了它们的促炎和细胞功能.
有效的瘤控制需要针对PD-1和PD-L1通路,以优化T细胞和TAM在TME中的相互作用.

关键词:

癌症癌症癌症癌症免疫学免疫学免疫学微观环境是一个微观环境.

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