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透瘤的CCR2+炎症单细胞抵消了特定免疫疗法的作用

Joschka Bartneck¹, Ann-Kathrin Hartmann¹, Lara Stein²

¹IIIrd Department of Medicine - Hematology, Oncology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.

Frontiers in immunology

|October 18, 2023

概括

DIVA2免疫平台通过促进细胞毒性CD8+T细胞有效控制瘤. 然而,免疫抑制单细胞 (CCR2+) 阻碍了这种反应,使它们成为改善癌症免疫治疗的目标.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
癌症研究癌症研究

背景情况:

瘤微环境 (TME) 极大地影响瘤的进展,涉及具有不同功能的多种免疫细胞.
像DIVA及其优化版本DIVA2这样的非侵入性免疫平台,提供针对瘤的治疗性疫苗接种策略.

研究的目的:

在MC38瘤模型中研究DIVA2的治疗效果.
阐明DIVA2免疫接种后TME内部的机制.

主要方法:

在MC38瘤模型中利用DIVA2的皮肤免疫.
采用高维流细胞计和单细胞mRNA测序来分析瘤透白细胞.
研究了CCR2+细胞通过抗体介导枯竭的作用.

主要成果:

由细胞毒性CD8+T细胞介导的DIVA2诱导的过渡性瘤控制.
观察到一种免疫逃避阶段,其特征是招募免疫抑制性CCR2+ PDL-1+单细胞.
消耗CCR2+细胞延长了生存时间,确定这些单细胞是瘤免疫逃生中的关键参与者.

结论:

DIVA2有效地产生抗原特异性T细胞反应,用于治疗癌症控制.
在TME中的免疫抑制性CCR2+单细胞抵消了DIVA2的疗效,是增强癌症免疫疗法的关键目标.

关键词:

CCR2单细胞 + CCR2单细胞癌症免疫疗法免疫疗法免疫逃避免疫逃避通过皮肤免疫接种.瘤微环境 (TME) 是指瘤的微环境.

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