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中枢神经系统原生骨髓细胞通过Cxcl10驱动大脑转移中的免疫抑制

Ian H Guldner¹, Qingfei Wang¹, Lin Yang²

¹Department of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN 46556, USA; Mike and Josie Harper Cancer Research Institute, University of Notre Dame, South Bend, IN 46617, USA.

|October 28, 2020

概括

中枢神经系统原生髓状细胞 (CNS- myeloids) 中Cx3cr1的损失通过产生免疫抑制位来促进大脑转移 (br- met). 这涉及Cxcl10介导的循环,增强了br-met的增长.

科学领域:

神经免疫学
癌症生物学
单细胞欧米体

背景情况:

大脑转移 (br-met) 发生在大脑中的一个独特的免疫.
中枢神经系统原生骨髓细胞 (CNS-myeloids) 和骨髓衍生骨髓细胞 (BMDMs) 相互作用调节大脑免疫力.
骨髓小组在br-met外生长中的具体作用和异质性尚不清楚.

研究的目的:

阐明中枢神经系统和BMDM子集在br-met中的表型异质性和功能作用.
确定驱动骨髓细胞介导的Br-met外生长的关键分子机制.

主要方法:

用多模式单细胞分析来研究br-met的骨髓细胞群.
使用基因操纵 (Cx3cr1淘汰) 和药理干预 (Cxcl10中和,VISTA/ PD- L1抑制) 来研究功能作用.

主要成果:

中枢神经神经质,而不是Ccr2+ BMDMs,促进了 br- met的增长.
中枢神经系统骨髓中Cx3cr1的下调导致br- met发生率增加,干扰素反应和Cxcl10的上调.
Cxcl10 中和降低了 br- met,而 rCxcl10 增加了 br- met,并招募了 VISTA+ PD- L1+ 中枢神经系统骨髓体.
抑制VISTA和PD- L1信号会降低免疫抑制和br- met负担.

结论:

中枢神经神经质中Cx3cr1的损失会启动一个由Cxcl10驱动的反循环,从而形成有利于br-met的免疫抑制环境.
针对Cxcl10-VISTA-PD-L1轴为治疗大脑转移提供了一个潜在的治疗策略.

关键词:

大脑转移一个T细胞来自骨髓的骨髓细胞大脑免疫力癌症免疫学免疫抑制免疫疗法发生转移的利基微质细胞瘤微环境

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