甲基强的松龙对多发性硬化免疫功能的影响

Effect of High dose Methylprednisolone Administration on Immune Functions in Multiple Sclerosis Patients

目的 通过计数细胞因子IFN γ和IL 10分泌细胞 ,检测多发性硬化 (MS)患者外周血单个核细胞IFN γ和IL 10分泌细胞水平 ,观察大剂量甲基强的松龙治疗对MS患者Th1及Th2细胞因子的影响。方法 将外周血单个核细胞暴露于中枢神经系统髓鞘素抗原髓鞘碱性蛋白进行体外短时间培养 ,用酶联免疫斑点试验(ELISPOT)检测IL 10和IFN γ分泌细胞 ,同时检测其他神经病组 (OND)及健康对照组。结果 显示MS患者IFN γ分泌细胞水平高于对照组 ,甲基强的松龙使MS患者IFN γ分泌细胞减少 ,对IL 10分泌细胞无明显影响。结论 MS患者存在Th1 Th2细胞因子的失衡 ,甲基强的松龙能抑制MSTh1类细胞因子IFN γ的产生 。

Objective Multiple sclerosis (MS) is postulated to be a Th1 type cell mediated autoimmune disease. Thus therapies that decrease T cell interferon (IFN) γ production or increase interleukin(IL) 10 production would be expected to have an ameliorating effect on MS. High doses of methylprednisolone(MP) are widely employed to treat acute attacks in MS patients. Their beneficial effects are partially due to their capacity to regulate the cytokine network. In the present work, we have examined the effect of MP on the production of the Immunosuppressor cytokine IL 10 and the inflammatory cytokine IFN γ. Methods Blood samples from MS patients suffering an acute relapse were obtained, levels of IL 10 and IFN γ secreting cells in PBMC were determined by ELISPOT, The expressions of IL 10 and IFN γ were studied in blood MNC of the MS patients after being cultured in the presence of myelin basic protein(MBP), or without MBP. Results In vitro experiments employing normal PBMC showed that MP downregulated both MBP induced IFN γ and spontaneous expression of IFN γ, and no effect on IL 10 secreting cells was found. Conclusion In summary, our results demonstrate a Th1 type cytokine bias in peripheral blood mononuclear cells of untreated MS patients that is reversed by MP treatment. These findings provide a basis for immune monitoring of patients with MS and suggest that treatments downregulating IFN γ may prove to be beneficial in progressive MS.