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在瘤微环境中的离子免疫抑制限制了T细胞效应器功能

Robert Eil¹, Suman K Vodnala¹, David Clever¹

¹National Cancer Institute, National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.

|September 15, 2016

概括

瘤缩释放,抑制T细胞的功能. 过度表达T细胞中的K_v1.3通道增强了抗瘤免疫力,并改善了黑色素瘤模型中的存活率.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
细胞生理学细胞生理学

背景情况:

尽管T细胞透,瘤的进展仍在发生.
瘤中的细胞亡与患者的生存率差相关.
亡会释放细胞内成分,可能会影响瘤的微环境.

研究的目的:

为了研究 necrosis 诱导的细胞外对 T 细胞功能的影响.
阐明介导的T细胞抑制背后的分子机制.
探索针对癌症免疫治疗的水平的治疗策略.

主要方法:

在小鼠和人类瘤中分析细胞外度 ([K+]e).
评估T细胞受体 (TCR) 驱动的Akt-mTOR酸化.
在体外和体内T细胞效应器程序的功能测试.
对T细胞进行遗传操纵,以过度表达通道K_v1.3.3.

主要成果:

来自的细胞外 ([K+]e) 含量升高抑制T细胞效应器功能.
高[K+]e通过酸酶PP2A损害了Akt-mTOR通过酸酶PP2A传递的信号.
抑制需要增加细胞内 ([K+]i),独立于血膜电位 (Vm).
在黑色素瘤模型中,K_v1.3的过度表达增强了T细胞功能和瘤清除.

结论:

结核诱发的高胆固醇血症会产生一种"离子检查点",抑制抗瘤T细胞的反应.
向流是增强癌症免疫疗法的新策略.
调节T细胞水平可以改善瘤根除和患者存活率.

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