FasL incapacitation alleviates CD4+ T cells-induced brain injury through remodeling of microglia polarization in mouse ischemic stroke

被引:21
作者
Zhao, Haoran [1 ,2 ]
Wan, Lihua [1 ,2 ]
Chen, Yan [1 ]
Zhang, He [1 ]
Xu, Yun [1 ,2 ]
Qiu, Shuwei [1 ,2 ]
机构
[1] Nanjing Univ, Sch Med, Drum Tower Hosp, Dept Neurol, Zhongshan Rd 321, Nanjing 210008, Jiangsu, Peoples R China
[2] Nanjing Univ, Sch Med, Jiangsu Key Lab Mol Med, Nanjing, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Ischemic stroke; CD4(+) T cells; Fas ligand; Microglia; NF-kappa B; CARDIAC XENOGRAFT SURVIVAL; FOCAL CEREBRAL-ISCHEMIA; NF-KAPPA-B; IMMUNE-RESPONSES; DEATH FACTOR; LIGAND GENE; ACTIVATION; INFLAMMATION; PATHWAY; DISEASE;
D O I
10.1016/j.jneuroim.2018.01.017
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammation responses involving the crosstalk between infiltrated T cells and microglia play crucial roles in ischemia stroke. Recent studies showed that Fas ligand (FasL) mutation could reduce post-stroke T cell invasion and microglia activation. In this study, we demonstrated that CD4(+) T cells could induce Ml microglia polarization through NF-KB signaling pathway, whereas FasL mutant CD4(+) T cells significantly reversed this effect. Besides, Th17/Treg cells balance was skewed into Treg cells after FasL mutation. In addition, conditioned medium from co culture of FasL mutant CD4(+) T cells and microglia could alleviate neuronal injury. Collectively, FasL incapacitation could alleviate CD4(+) T cells-induced inflammation through remodeling microglia polarization, suggesting a therapeutic potential for control of inflammation responses after ischemic stroke.
引用
收藏
页码:36 / 44
页数:9
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