实验性变应性脑脊髓炎髓鞘脱失机制的研究  

Research on demyelinating mechanism in acute experimental allergic encephalomyelitis in cynomolgus monkeys

作　　者：胡学强[1] 陆正齐[1] 邱伟[1] 

机构地区：[1]中山大学附属第三医院神经科,广州510630

出　　处：《中国免疫学杂志》2004年第3期180-183,共4页Chinese Journal of Immunology

基　　金：国家自然科学基金资助 (No .92 70 2 75 )

摘　　要：目的 :探讨自身免疫性脱髓鞘疾病的中枢神经系统 (CNS)髓鞘脱失发生机制。方法 :采用同源脑白质匀浆建立猴实验性变应性脑髓炎 (EAE)模型 ,并用流式细胞仪检测血和脑脊液淋巴细胞亚群的变化 ,用免疫组化技术和电镜观察脑组织病理变化。结果 :急性EAE猴脑脊液CD4 + T淋巴细胞明显升高 ,CD8+ T淋巴细胞和B淋巴细胞轻度升高 ;颞叶深部白质有大量CD4 + T淋巴细胞和少量CD8+ T淋巴细胞浸润 ,而对照组均未见变化 ;髓鞘内板层松解和轴突髓鞘分离 ,而髓鞘外板层正常 ,轴突也保存完好 ,少突胶质细胞 (ODC)的部分胞浆明显水肿 ,线粒体肿胀 ,嵴模糊或断裂 ,核部分溶解。结论 :提示EAE脱髓鞘免疫因子最早攻击的靶是少突胶质细胞 ,而不是髓鞘本身。Objective:To study demyelinating mechanism of the central nervous system in acute experimental allergic encephalomyelitis(EAE).Methods:EAE in cynomolgus monkeys was induced successfully by homologous brain white matter homogenate. Lymphocyte subset in blood and cerebrospinal fluid was monitored by flow cytometer. Pathological changes in brains of acute EAE monkeys were investigated by immunohistochemistry and electron microscopy. Results:In the CSF of acute EAE, CD4 + lymphocytes increased significantly, and CD8 + lymphocytes and B lymphocytes increased slightly whereas the control was normal. A lot of CD4 + lymphocytes and a few CD8 + lymphocytes infiltrated into temporal deep white matter of acute EAE, whereas the control was normal. Inner laminae of myelin sheath were loose and axon was separated, whereas outer laminae were normal. Although axon was preserved well, oligodendrocyte had a severe edema in cytoplasm with mitochondria swollen, crista blurred or broken, and nucleus lysised partly.Conclusion:It is oligodendrocyte rather than myelin sheath itself which is firstly attacked in the demyelination in EAE.

关 键 词：食蟹猴 实验性变态反应性脑髓炎 髓鞘脱失 机制 

分 类 号：R744.5[医药卫生—神经病学与精神病学]