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PD-1/PD-L1 Axis as a Potential Therapeutic Target for Multiple Sclerosis: A T Cell Perspective

期刊

FRONTIERS IN CELLULAR NEUROSCIENCE
卷 15, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2021.716747

关键词

experimental autoimmune encephalomyelitis; multiple sclerosis; T cells; programmed cell death ligand-1; programmed cell death protein-1

资金

  1. General Program of the National Natural Science Foundation of China [81671177]
  2. Natural Science Foundation of Jilin Province Science and Technology Development Plan Project [20190201043JC]
  3. Key Research and Development Project of Social Development Division of Jilin Science and Technology Department [20200403109SF]
  4. Special Project for Health Professionals of Jilin Provincial Finance Department [JLSWSRCZX20200056]
  5. Swedish Research Council [2015-03005]
  6. Jilin University of China
  7. Swedish Research Council [2015-03005] Funding Source: Swedish Research Council

向作者/读者索取更多资源

The PD-1/PD-L1 axis plays a crucial role in multiple sclerosis (MS), and understanding the complex relationship between them may expand our knowledge of therapeutic approaches.
The programmed cell death protein-1/programmed death ligand-1 (PD-1/PD-L1) axis is a widely studied immune checkpoint that modulates signaling pathways related to T cell activation. The use of PD-1/PD-L1 inhibitors is a promising immune therapy strategy for cancer patients. However, individuals treated with PD-1/PD-L1 inhibitors may develop immune-related adverse events due to excessive immune reactions. Multiple sclerosis (MS) is a chronic demyelinating and neurodegenerative disease of the central nervous system. T cells and the PD-1/PD-L1 axis play vital roles in the pathogenesis of MS. A better understanding of the complex relationship between the PD-1/PD-L1 axis and T cells may extend our knowledge of the molecular mechanisms and therapeutic approaches for MS. In this review, we summarize the most recent findings regarding the role of the PD-1/PD-L1 axis in MS and discuss the potential therapeutic strategies to modulate the expression of PD-1/PD-L1 in MS.

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