Methylprednisolone is an effective drug in the treatment of autoimmune disease, such as multiple sclerosis (MS), due to long‐acting anti‐inflammatory, antiallergic and immunosuppressant. Previous studies have noted the importance of myeloid‐derived suppressor cells (MDSC) in MS progression. However, it is still not known whether methylprednisolone could influence the ratio and function of MDSC during MS treatment. In the current study, we found an increased ratio of MDSC at the onset of EAE in mice model; but methylprednisolone pulse therapy (MPPT) did not alter the percentage and suppressive function of MDSC during disease attenuation. However, the percentage of G‐MDSC in PBMC significantly increased in patients with MS. Surprisingly, relapsing MS patients showed a significant increase in both M‐MDSC and G‐MDSC after MPPT. The disease remission positively correlated expansion of MDSC and expression of arginase‐1. Additionally, MPPT reduced the expression of inhibitory glucocorticoid (GCs) receptor β subunit on MDSC while elevating serum levels of immune regulatory S100A8/A9 heterodimer. Thus, MDSC dynamics and function in mouse EAE differ from those in human MS during MPPT. Our study suggested that GCs treatment may help relieve the acute phase of MS by expanding MDSC through up‐regulating of GR signalling and S100A8/A9 heterodimers.

中文翻译：

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甲基强的松龙通过糖皮质激素受体 β 和 S100A8/9 上调扩增髓源性抑制细胞减轻多发性硬化症

由于长效抗炎、抗过敏和免疫抑制剂，甲基强的松龙是治疗多发性硬化症（MS）等自身免疫性疾病的有效药物。先前的研究已经注意到髓源性抑制细胞 (MDSC) 在 MS 进展中的重要性。然而，目前尚不清楚甲基强的松龙是否会影响 MS 治疗期间 MDSC 的比例和功能。在目前的研究中，我们发现小鼠模型中 EAE 发作时 MDSC 的比例增加；但甲基强的松龙冲击疗法 (MPPT) 在疾病衰减期间并未改变 MDSC 的百分比和抑制功能。然而，在 MS 患者中，PBMC 中 G-MDSC 的百分比显着增加。令人惊讶的是，复发的 MS 患者在 MPPT 后 M-MDSC 和 G-MDSC 均显着增加。疾病缓解与 MDSC 扩增和 arginase-1 表达呈正相关。此外，MPPT 降低了 MDSC 上抑制性糖皮质激素 (GCs) 受体 β 亚基的表达，同时提高了免疫调节 S100A8/A9 异二聚体的血清水平。因此，在 MPPT 期间，小鼠 EAE 中的 MDSC 动力学和功能与人类 MS 中的不同。我们的研究表明，GCs 治疗可能通过上调 GR 信号和 S100A8/A9 异二聚体来扩大 MDSC，从而帮助缓解 MS 的急性期。