实验性自身免疫性重症肌无力小鼠免疫功能状态的研究

目的：探讨实验性自身免疫性重症肌无力（EAMG）模型小鼠免疫应答特点。方法：根据临床症状及重复电刺激试验结果将造模小鼠分为成模组及未成模组,检测其免疫功能状态的改变,包括血清中乙酰胆碱受体抗体（AchRab）的水平,脾脏CD4^＋T细胞数量,用淋巴细胞增殖试验检测脾细胞经刀豆蛋白A（ConA）活化的非特异增殖能力,检测脾脏T细胞因子白细胞介素4（IL-4）,干扰素γ（IFN-γ）分泌水平。并与弗氏佐剂（CFA）对照组及正常对照组进行比较。结果：与未成模组、弗氏佐剂对照组及正常对照组相比,成模组小鼠AchRab显著增高,脾脏CD4^＋T细胞数升高;外周脾细胞对ConA刺激的非特异性增殖能力显著升高;脾脏T细胞细胞因子IL-4,IFN-γ显著升高,（均P〈0.01）,IFN-γ升高的程度高于IL-4（P〈0.01）。结论：EAMG发生是一个自身免疫应答参与的过程,体液免疫、细胞免疫应答参与了EAMG的发生。

STUDY ON IMMUNE STATE OF EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS MICE

Objective.To study the changes of immune state in EAMG mice. Methods. The model mice were divided into MG symptom group and no MG symptom group by clinical manifestation and repetitive nerve stimulation. The changes of immune function in model mice were tested and compared with control group. The changes of immune function included determination of anti-AchR antibodies, frequency of CD4^＋T cells in spleen, the nonspecific proliferation ability of splenocyte to the stimulation with ConA respectively, the level of cytokine IL-4,IFN-γ secreted by T cells in spleen. Result：Compared with no MG symptom group, CFA group and control group, MG symptom group serum anti-AchR antibodies increased significantly. The level of CD4^＋T cells increased, while the nonspecific proliferation ability of splenocyte increased significantly. The level of cytokine IL-4, IFN-γ secreted by T cells in spleen increased. Compared with IL-4, IFN-γ increased markedly. Conclusion：The development of disease is a process of autoimmune response. It suggested that humoral immune and cellular immune involved in the development of EAMG.