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Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Programmed Death Ligand-1 on Microglia Regulates Th1 Differentiation via Nitric Oxide in Experimental Autoimmune
Jingxia Hu1,2, Hao He2, Zhengang Yang3
1College of Life Science, Shandong Agricultural University, Taian, 271018, China.
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.
Insights
Microglia suppress T cell responses in experimental autoimmune encephalomyelitis (EAE) by up-regulating programmed death ligand-1 (PD-L1), inhibiting Th1 cell differentiation via nitric oxide (NO). This highlights microglia
Area of Science:
- Neuroimmunology
- Cellular immunology
Background:
- Microglia, the immune cells of the central nervous system, are implicated in antigen presentation during disease.
- The precise role of microglia in immune regulation, particularly in autoimmune conditions, remains incompletely understood.
Purpose of the Study:
- To investigate the suppressive activity of microglia in experimental autoimmune encephalomyelitis (EAE).
- To elucidate the mechanisms by which microglia regulate T cell responses during EAE.
Main Methods:
- Induction of EAE using myelin oligodendrocyte glycoprotein.
- Flow cytometric analysis of microglia and T cells in the central nervous system.
- Ex vivo co-culture systems with microglia and T cells.
- Inhibition studies using PD-L1 blockade and nitric oxide (NO) assessment.
Main Results:
- Microglia numbers and programmed death ligand-1 (PD-L1) expression increased in EAE.
- Upregulated PD1 on T cells and microglia correlated with decreased Th1 cells.
- Microglia from EAE mice inhibited CD4+ T cell proliferation and Th1 differentiation.
- PD-L1 blockade reversed microglia-mediated suppression.
- Microglia suppressed Th1 cells through PD-L1-dependent nitric oxide (NO) production.
Conclusions:
- Microglia play a regulatory role in EAE by suppressing Th1 cell differentiation.
- The PD-L1-NO pathway is a key mechanism mediating microglia-induced suppression in EAE.
- Targeting the PD-L1-NO pathway in microglia may offer therapeutic strategies for EAE.
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