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CD4(+)T cell specific B7-H1 selectively inhibits proliferation of naïve T cells and Th17 differentiation in experimental autoimmune encephalomyelitis

It is widely acknowledged that interleukin 17-producing T helper (Th17) cells are critically participant in the pathogenesis of multiple sclerosis. In the current study, we identified that the expression of CD4(+)T cells specific co-inhibitory molecule B7-homologue 1(B7-H1) in spleenocytes and monon...

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Detalles Bibliográficos
Autores principales: Shi, Sheng-Jia, Ding, Mei-Ling, Wang, Li-Juan, Wu, Jie-Heng, Han, Dong-Hui, Zheng, Guo-Xu, Guo, Zhang-Yan, Xi, Wen-Jin, Qin, Wei-Jun, Yang, An-Gang, Wen, Wei-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5685729/
https://www.ncbi.nlm.nih.gov/pubmed/29163808
http://dx.doi.org/10.18632/oncotarget.21357
Descripción
Sumario:It is widely acknowledged that interleukin 17-producing T helper (Th17) cells are critically participant in the pathogenesis of multiple sclerosis. In the current study, we identified that the expression of CD4(+)T cells specific co-inhibitory molecule B7-homologue 1(B7-H1) in spleenocytes and mononuclear cells isolated from brains and spinal cord were positive correlated with Th1 and Th17 cells generation and disease severity in experimental autoimmune encephalomyelitis (EAE). Furthermore, B7-H1 transgenic mice developed milder EAE symptoms and fewer Th17 cells than B7-H1 wild type mice. We also found the proliferation of naïve CD4(+)CD62(+)T cells isolated from B7-H1 transgenic mice was inhibited. And naïve T cells isolated from B7-H1 transgenic mice produced fewer Th17 cells than WT mice in Th17-polarizing conditions, but the Th1, Th2, and inducible Treg differentiation were the similar in naïve T cells isolated from B7-H1 transgenic mice and WT mice. In conclusion, our study show CD4(+)T cells specific B7-H1 is a slective inhibitor in proliferation of naïve T cells, Th17 differentiation and pathogenesis of multiple sclerosis.