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通过CD8+T细胞的PD1阻塞诱导的DKK1表达促进了血脑屏障的透.

Abhilash Deo¹, Sapir Levin¹, Chen Buxbaum¹

¹Technion - Israel Institute of Technology Haifa Israel.

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概括

抗PD1疗法可以通过DKK1表达T细胞破坏血脑屏障 (BBB),影响大脑转移 (BrM) 治疗. 针对这种BBB漏洞可能会提高BrM的免疫疗法疗效.

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科学领域:

神经瘤学神经瘤学
免疫治疗是一种免疫疗法.
癌症生物学癌症生物学

背景情况:

抗PD1疗法对一些大脑转移 (BrM) 患者有好处,但反应异质性表明理解大脑的免疫环境存在差距.
现有的研究缺乏明确的宿主特异性因素,这些因素影响了BrM中对免疫检查点抑制剂 (ICI) 的可变反应.

研究的目的:

研究大脑转移中对抗PD1治疗的可变反应的宿主驱动决定因素.
描述大脑微环境的免疫格局及其与抗PD1治疗的相互作用.

主要方法:

单细胞RNA测序被用来分析大脑微环境对抗PD1治疗的反应.
研究了通过抗PD1疗法调节血脑屏障 (BBB) 完整性的机制.
在患者中评估了血DKK1水平和MRI对比度增强.

主要成果:

抗PD1疗法诱导了显著的抗瘤免疫激活,但独特地损害了BBB完整性.
通过特定的分子通路,鉴定出表达DKK1的活性CD8+T细胞是BBB透的媒介.
临床数据显示,在接受抗PD1的患者中,MRI对比度增强,DKK1水平与非响应者的BrM发生率相关.
与抗PD1和西斯普拉丁的联合治疗增强了ICI耐药BrM的药物递送和疗效.

结论:

抗PD1疗法可以调节BBB完整性,在大脑转移管理中呈现潜在的脆弱性.
针对DKK1介导的BBB干扰提供了一种新的治疗策略,以提高对大脑转移的免疫疗法疗效.
连续的抗PD1和西斯普拉丁治疗显示出克服BRM中ICI耐药性的希望.