Immune Modulatory Effects of PD-1/PD-L1 in Myasthenia Gravis: Insights From Peripheral Blood Mononuclear Cell Analysis.

PD-1/PD-L1在重症肌无力中的免疫调节作用:来自外周血单核细胞分析的启示

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作者:Li Jianing, Liu Xinyue, Qi Feiteng, Ren Yan, Zhang Yuanting, Shen Yaoyang, Liu Hua, Wang Yixuan, Zheng Rou, Ou Yangxiang, Wang Geng, Li Na
Myasthenia gravis (MG) is an autoimmune disease characterized by the production of antibodies targeting acetylcholine receptor (AChR)-associated proteins. The disorder involves various immune cells, including T cells, B cells, and dendritic cells (DCs). Programmed cell death protein 1 (PD-1) is one of the immune checkpoints and plays a crucial role in regulating immune cell activation and cell death. PD-L1, the ligand of PD-1, is critical for immune suppression through the transmission of inhibitory signals. These molecules are implicated in the pathogenesis of MG, prompting further investigation into the expression and functional roles of PD-1/PD-L1 in this disease. To investigate the role of PD-1/PD-L1 in MG pathogenesis, we collected peripheral blood mononuclear cells (PBMCs) from MG patients and analyzed PD-1/PD-L1 expression in various immune cells using flow cytometry (FACs). Our findings revealed that PD-1/PD-L1 expression was elevated in PBMCs from MG patients compared to healthy controls. We conducted a correlation analysis to examine the relationship between PD-1/PD-L1 expression and MG, based on measurements of anti-AChR-IgG levels, MG-specific cytokines, and routine blood tests. Our results showed that PD-1 expression in CD8(+) T cells and PD-L1 expression in DCs were positively correlated with anti-AChR-IgG levels in MG serum. Additionally, PD-1/PD-L1 expression was correlated with parts of associated cytokines. Furthermore, PD-1 expression in B cells was positively correlated with lymphocyte counts in the peripheral blood. Moreover, exogenous recombinant human PD-L1 protein (rhPDL1) was found to suppress the expression of IL-1β and IL-4. Our findings underscore the potential therapeutic role of PD-1/PD-L1 agonists in the treatment of MG.

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