医学
细胞毒性T细胞
细胞凋亡
癌症研究
Fas配体
细胞生物学
冲程(发动机)
免疫学
CD8型
细胞毒性
神经科学
生物
程序性细胞死亡
免疫系统
体外
生物化学
工程类
机械工程
作者
Lizhen Fan,Cun‐Jin Zhang,Liwen Zhu,Jian Chen,Zhi Zhang,Pinyi Liu,Xiang Cao,Hailan Meng,Yun Xu
标识
DOI:10.1007/s12975-019-00749-0
摘要
CD8+ T cells are recognized as key players in exacerbation of ischemic stroke; however, the underlying mechanism in modulating the function of CD8+ T cells has not been completely elucidated. Here, we uncovered that FasL enhanced the cytotoxicity of CD8+ T cells to neurons after ischemic stroke. Inactivation of FasL specific on CD8+ T cells protected against brain damage and neuron loss. Proteomic analysis identified that PDPK1 functioned downstream of FasL signaling and inhibition of PDPK1 effectively reduced cytotoxicity of CD8+ T cells and improved ischemic neurological deficits. Taken together, these results highlight an intrinsic FasL-PDPK1 pathway regulating the cytotoxicity of CD8+ T cells in ischemic stroke.
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