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Published in: Neuroscience Bulletin 1/2016

01-02-2016 | Original Article

Programmed Death Ligand-1 on Microglia Regulates Th1 Differentiation via Nitric Oxide in Experimental Autoimmune Encephalomyelitis

Authors: Jingxia Hu, Hao He, Zhengang Yang, Guangming Zhu, Li Kang, Xiuli Jing, Hai Lu, Wengang Song, Bo Bai, Hua Tang

Published in: Neuroscience Bulletin | Issue 1/2016

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Abstract

Microglia are considered to be potential antigen-presenting cells and have the ability to present antigen under pathological conditions. Nevertheless, whether and how microglia are involved in immune regulation are largely unknown. Here, we investigated the suppressive activity of microglia during experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein, with the goal of understanding their role in regulating the T cell reaction. Using flow cytometric analysis, we found that microglia were characterized by increased cell number and up-regulated programmed death ligand-1 (PD-L1) at the peak phase of EAE. Meanwhile, both the CD4+ T cells and microglia that infiltrated the central nervous system expressed higher levels of PD1, the receptor for PD-L1, accompanied by a decline of Th1 cells. In an ex vivo co-culture system, microglia from EAE mice inhibited the proliferation of antigen-specific CD4+ T cells and the differentiation of Th1 cells, and this was significantly inhibited by PD-L1 blockade. Further, microglia suppressed Th1 cells via nitric oxide (NO), the production of which was dependent on PD-L1. Thus, these data suggest a scenario in which microglia are involved in the regulation of EAE by suppressing Th1-cell differentiation via the PD-L1-NO pathway.
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Metadata
Title
Programmed Death Ligand-1 on Microglia Regulates Th1 Differentiation via Nitric Oxide in Experimental Autoimmune Encephalomyelitis
Authors
Jingxia Hu
Hao He
Zhengang Yang
Guangming Zhu
Li Kang
Xiuli Jing
Hai Lu
Wengang Song
Bo Bai
Hua Tang
Publication date
01-02-2016
Publisher
Springer Singapore
Published in
Neuroscience Bulletin / Issue 1/2016
Print ISSN: 1673-7067
Electronic ISSN: 1995-8218
DOI
https://doi.org/10.1007/s12264-015-0010-9

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