Journal
MOLECULAR NEUROBIOLOGY
Volume 58, Issue 12, Pages 6249-6271Publisher
SPRINGER
DOI: 10.1007/s12035-021-02495-7
Keywords
PD-1; PD-L1; Multiple sclerosis; Experimental autoimmune encephalomyelitis; Immune tolerance
Categories
Funding
- General Program of the National Natural Science Foundation of China [81671177]
- Natural Science Foundation of Jilin Province Science and Technology Development Plan Project [20190201043JC]
- Key Research and Development Project of Social Development Division of Jilin Science and Technology Department [20200403109SF]
- Special Project for Health Professionals of Jilin Provincial Finance Department [JLSWSRCZX2020-0056]
- Swedish Research Council [2015-03005]
- Jilin University of China
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PD-1/PD-L1 signaling plays a crucial role in multiple sclerosis by blocking autoimmune responses, maintaining immune tolerance, and inhibiting autoimmunity. Therefore, PD-1/PD-L1 has the potential to serve as biomarkers or therapeutic targets for multiple sclerosis.
Multiple sclerosis (MS) is an autoimmunity-related chronic demyelination disease of the central nervous system (CNS), causing young disability. Currently, highly specific immunotherapies for MS are still lacking. Programmed cell death 1 (PD-1) is an immunosuppressive co-stimulatory molecule, which is expressed on activated T lymphocytes, B lymphocytes, natural killer cells, and other immune cells. PD-L1, the ligand of PD-1, is expressed on T lymphocytes, B lymphocytes, dendritic cells, and macrophages. PD-1/PD-L1 delivers negative regulatory signals to immune cells, maintaining immune tolerance and inhibiting autoimmunity. This review comprehensively summarizes current insights into the role of PD-1/PD-L1 signaling in MS and its animal model experimental autoimmune encephalomyelitis (EAE). The potentiality of PD-1/PD-L1 as biomarkers or therapeutic targets for MS will also be discussed.
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