PDF(Pubmed)
Abstract：
Peripheral immune cells infiltrating into the brain trigger neuroinflammation after an ischemic stroke. Partial immune cells reprogram their function for neural repair. Which immune cells promote ischemic brain recovery needs further identification.
We performed single-cell transcriptomic profiling of CD45high immune cells isolated from the ischemic hemisphere at subacute (5 days) and chronic (14 days) stages after ischemic stroke.
A subset of phagocytic macrophages was associated with neuron projection regeneration and tissue remodeling. We also identified a unique type of T cells with highly expressed macrophage markers, including C1q, Apoe, Hexb, and Fcer1g, which showed high abilities in tissue remodeling, myelination regulation, wound healing, and anti-neuroinflammation. Moreover, natural killer cells decreased cytotoxicity and increased energy and metabolic function in the chronic stage after ischemic stroke. Two subgroups of neutrophils upregulated CCL signals to recruit peripheral immune cells and released CXCL2 to keep self-recruiting at the chronic stage.
We identified subsets of peripheral immune cells that may provide potential therapeutic targets for promoting poststroke recovery.
We performed single-cell transcriptomic profiling of CD45high immune cells isolated from the ischemic hemisphere at subacute (5 days) and chronic (14 days) stages after ischemic stroke.
A subset of phagocytic macrophages was associated with neuron projection regeneration and tissue remodeling. We also identified a unique type of T cells with highly expressed macrophage markers, including C1q, Apoe, Hexb, and Fcer1g, which showed high abilities in tissue remodeling, myelination regulation, wound healing, and anti-neuroinflammation. Moreover, natural killer cells decreased cytotoxicity and increased energy and metabolic function in the chronic stage after ischemic stroke. Two subgroups of neutrophils upregulated CCL signals to recruit peripheral immune cells and released CXCL2 to keep self-recruiting at the chronic stage.
We identified subsets of peripheral immune cells that may provide potential therapeutic targets for promoting poststroke recovery.
摘要：
目的：外周免疫细胞浸润到脑内引发缺血性卒中后的神经炎症。部分免疫细胞重新编程其功能以进行神经修复。哪些免疫细胞促进缺血脑恢复有待进一步鉴定。
方法：我们对缺血性卒中后亚急性（5天）和慢性（14天）阶段分离自缺血半球的CD45high免疫细胞进行了单细胞转录组学分析。
结果：吞噬巨噬细胞亚群与神经元投射再生和组织重塑有关。我们还鉴定了一种具有高表达巨噬细胞标记的独特类型的T细胞，包括C1q,Apoe,Hexb,和Fcer1g,表现出很高的组织重塑能力，髓鞘形成调节,伤口愈合，和抗神经炎症。此外，在缺血性卒中后的慢性期，自然杀伤细胞的细胞毒性降低，能量和代谢功能增加。中性粒细胞的两个亚组上调CCL信号以募集外周免疫细胞并释放CXCL2以在慢性期保持自我募集。
结论：我们鉴定了可能为促进卒中后恢复提供潜在治疗靶点的外周免疫细胞亚群。
方法：我们对缺血性卒中后亚急性（5天）和慢性（14天）阶段分离自缺血半球的CD45high免疫细胞进行了单细胞转录组学分析。
结果：吞噬巨噬细胞亚群与神经元投射再生和组织重塑有关。我们还鉴定了一种具有高表达巨噬细胞标记的独特类型的T细胞，包括C1q,Apoe,Hexb,和Fcer1g,表现出很高的组织重塑能力，髓鞘形成调节,伤口愈合，和抗神经炎症。此外，在缺血性卒中后的慢性期，自然杀伤细胞的细胞毒性降低，能量和代谢功能增加。中性粒细胞的两个亚组上调CCL信号以募集外周免疫细胞并释放CXCL2以在慢性期保持自我募集。
结论：我们鉴定了可能为促进卒中后恢复提供潜在治疗靶点的外周免疫细胞亚群。
