Multiple sclerosis (MS) is a complex inflammatory and demyelinating disease of the central nervous system (CNS) frequently starts in young adulthood. Demyelination, inflammatory and axonal damage in the CNS is the pathological hallmark of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. 1, 25-dihydroxyvitamin D3 (Vitamin D3) is involved in calcium regulation, phosphorus homeostasis, and bone mineralization. In addition, vitamin D3 has potential inhibitory effects on immune cells in various inflammatory and autoimmunity disease. C57BL/6 female mice were divided into prevention groups (low, middle and high doses) and treatment groups (middle and high doses). Prevention groups received vitamin D3 2 weeks before EAE induction, and treatment groups were treated with vitamin D3 simultaneous with EAE induction. Vitamin D3 inhibits the development of EAE in a dose-dependent manner. Histological studies revealed reduced demyelination and limited infiltration into CNS, moreover vitamin D3 increased the production of IL-4, IL-10, and TGF-β, while a significant reduction in the production of IFN-γ, IL-6, TNF-α, and IL-17 was observed. Flow cytometry results for CD4+ T cell subsets in compliance with ELISA cytokine assay results showed a significant decrease in the percentage of Th1 and Th17, but also a significant increase in the percentage of Th2 and Treg for middle and high dose vitamin D3 treated mice. Real-time PCR results indicated that middle and high dose vitamin D3 treatment reduced T-bet and ROR-γt expression, but enhanced GATA3 and Foxp3 expression. Real-Time PCR results in CNS for T cell subsets related cytokines and transcription factors supported the results of flow cytometry and ELISA. This study indicated that middle and high doses of vitamin D3 deviate the balance between Th1/Th2 and Th17/Treg to Th2 and Treg. Moreover, vitamin D3 could reduce the incidence and severity of EAE clinical disease.

中文翻译：

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用1，25-二羟基维生素D3预防和治疗实验性自身免疫性脑脊髓炎小鼠。

多发性硬化症（MS）是中枢神经系统（CNS）的一种复杂的炎症性和脱髓鞘性疾病，通常在成年后开始。中枢神经系统的脱髓鞘，炎症和轴突损伤是实验性自身免疫性脑脊髓炎（EAE）（一种多发性硬化症的动物模型）的病理特征。1，25-二羟基维生素D3（维生素D3）与钙调节，磷稳态和骨骼矿化有关。此外，维生素D3对各种炎症和自身免疫性疾病的免疫细胞具有潜在的抑制作用。将C57BL / 6雌性小鼠分为预防组（低，中和高剂量）和治疗组（中和高剂量）。预防组在诱发EAE前2周接受维生素D3，治疗组在诱发EAE的同时接受维生素D3治疗。维生素D3以剂量依赖性方式抑制EAE的发展。组织学研究表明，脱髓鞘减少和对CNS的浸润有限，而且维生素D3增加了IL-4，IL-10和TGF-β的产生，而IFN-γ，IL-6，TNF-α的产生则显着减少，并且观察到IL-17。与ELISA细胞因子检测结果相符的CD4 + T细胞亚群的流式细胞仪结果显示，对于中，高剂量维生素D3处理的小鼠，Th1和Th17的百分比显着降低，但Th2和Treg的百分比也显着提高。实时PCR结果表明，中高剂量维生素D3处理可降低T-bet和ROR-γt表达，但可增强GATA3和Foxp3表达。CNS中T细胞亚群相关细胞因子的实时PCR结果，转录因子支持流式细胞仪和ELISA的结果。这项研究表明，中等剂量和高剂量的维生素D3会偏离Th1 / Th2和Th17 / Treg与Th2和Treg之间的平衡。此外，维生素D3可以降低EAE临床疾病的发生率和严重程度。