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重症肌无力患者免疫发病机理的研究
引用本文:赖祥青,杨明山,徐金枝,唐荣华,高波廷. 重症肌无力患者免疫发病机理的研究[J]. 中国病理生理杂志, 2001, 17(7): 662-664
作者姓名:赖祥青  杨明山  徐金枝  唐荣华  高波廷
作者单位:1. 暨南大学医学院第一附属医院神经内科, 广东广州 510630;
2. 同济医科大学附属同济医院神经科, 湖北武汉 430030
摘    要:目的:进一步探讨重症肌无力(MG)的发病机理。方法:用ELISA法对285例MG病人进行AchRab和PsMab的检测。同时还检测202例MG病人的TNF-α、RBC-C3bRR和RBC-ICR及104例MG病人外周血淋巴细胞亚群。结果:MG患者AchRab和PsMab的阳性率均明显高于对照组。AchRab阴性组的PsMab阳性率明显高于AchRab阳性组;202例MG患者的TNF-α显著高于对照组;RBC-C3bRR明显低于对照组,而RBC-ICR则与对照组无显著差异。104例MG病人的T8+细胞明显低于对照组,T4/T8比值则高于对照组。结论:MG是一种以AchRab损害突触后膜为主的自身免疫性疾病,部分AchRab和PsMab均阳性的病人可能同时有突触前膜和突触后膜的损害;而AchRab阴性PsMab阳性的病人可能以突触前膜的损害为主,两抗体均阴性的病人可能是细胞免疫或/和TNF-α等其他体液免疫所致。

关 键 词:重症肌无力  受体  胆碱能  抗体  突触膜  肿瘤坏死因子  
文章编号:1000-4718(2001)07-0662-03
收稿时间:2000-11-16
修稿时间:2000-11-16

Study on the immunologic mechanism of myasthenia gravis
LAI Xiang-qing ,YANG Ming-shang ,XU Jin-zhi ,TANG Rong-hua ,GAO Bo-ting. Study on the immunologic mechanism of myasthenia gravis[J]. Chinese Journal of Pathophysiology, 2001, 17(7): 662-664
Authors:LAI Xiang-qing   YANG Ming-shang   XU Jin-zhi   TANG Rong-hua   GAO Bo-ting
Affiliation:1. Department of Neurology, the First Affiliated Hospital, Medical College of Jinan University,Guangzhou 510630,China;
2. Department of Neurology, Tongji Hospital of Tongji Medical University, Wuhan 430030, China
Abstract:AIM: To further investigate the immunologic mechanism of myasthenia gravis(MG). METHODS: Acetylcholine receptor antibodies(AchRab) and presynaptic membrane antibodies (PsMab) was determined by ELISA in 285 cases of MG patients. Tumor necrosis factor- alpha(TNF-α) and RBC-C3b receptor rosette rate(RBC-C3bRR)and RBC-IC rosette rate (RBC-ICR)was determined in 202 patients with MG. Furthermore, the peripheral blood lymphocyte subsets was examined in 104 cases MG patients. RESULTS: The positive rates of the AchRab and PsMab in MG were very significantly higher than that of control.The positive rate of PsMab in patients with negative AchRab was very significantly higher than that of patients with the positive AchRab.In 202 MG patients, the TNF-α was significantly higher, but the RBC-C3bRR was significantly lower than those of control, while the RBC-ICR has no significant change. CONCLUSION: MG is an autoimmune disease with damaged postsynaptic membrane by the AchRab, and some patients with both the AchRab and PsMab could manifest disfunction in the postsynaptic and presynaptic membrane. While the patients who just has the PsMab maybe damaged only in the presynaptic membrane. Other body fluid immune or/and cell immune mechanism may be involved in MG patients without AchRab and PsMab.
Keywords:Myasthenia gravis  Receptors   cholinergic  Antibodies  Synaptic membranes  Tumor necrosis factor
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