Abstract
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.
Highlights
Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination, axonal injury, and neuronal loss in the central nervous system (CNS), causing a variety of clinical symptoms involving motor, sensory, visual, and autonomic systems (Dobson and Giovannoni, 2019)
The regulatory effects of soluble PD-1 (sPD-1)/soluble PD-L1 (sPD-L1) in autoimmune diseases and tumors have been reported in previous studies (Table 1). They found that the expression of sPD-1/sPD-L1 was upregulated in patients with autoimmune diseases compared with healthy subjects, but downregulated after treatment, suggesting that sPD-1 may resist the inhibitory effect of membrane-bound PD1 on T cells, thereby indirectly enhancing immune responses
SPD-1 blocked the inhibitory effect of membrane-bound PD-1 on T cell activation, and induced the Th1/Th17 immune response sPD-1 aggravated the severity of rheumatoid arthritis (RA)
Summary
Multiple sclerosis (MS) is an autoimmune disease characterized by demyelination, axonal injury, and neuronal loss in the central nervous system (CNS), causing a variety of clinical symptoms involving motor, sensory, visual, and autonomic systems (Dobson and Giovannoni, 2019). The activation of the PD-1 gene is involved in programmed cell death and can promote the evasion of tumor cells from effective immune responses. We propose that the activation of a variety of immune cells induces the production of proinflammatory cytokines during the relapsing phase of MS, and promotes the expression of PD1/PD-L1.
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