FINE STRUCTURAL PATHOLOGY OF MYELIN

在两种病毒中研究了脱髓鞘和重髓鞘形成的机制。 电子学方法诱导(SJL/Balb/c)F1小鼠脱髓鞘疾病 显微镜、免疫荧光和放射自显影。实验性的 任一小鼠肝炎所致的小鼠白质脑脊髓炎模型 泰勒氏小鼠脑脊髓炎病毒(DAV)的病毒(MHV)或DA株。 目的是：1)确定T淋巴细胞亚群 炎性脱髓鞘病变在疾病的不同阶段和 将它们的分布与过敏性皮损进行比较 脑脊髓炎(EAE)。2)测定脾细胞的超敏反应 抗小鼠脊髓匀浆、髓鞘碱性蛋白的细胞 (MBP)，并在DAV诱导的脱髓鞘过程中灭活DAV。 3)移植小鼠的淋巴和脾细胞 DAV感染后脑白质病变的发展及寻找 以受体小鼠为阳性对照的组织学损害 从感染EAE的小鼠身上转移淋巴样细胞。4)学习 免疫球蛋白产生杂交瘤小鼠的记忆功能 在从MHV感染中恢复期间。预计这一发现将 有助于理解人类感染后肺炎的发病机制 脑脊髓炎和多发性硬化症。

Mechanisms of demyelination and remyelination are studied in two virus induced demyelinating diseases in (SJL/Balb/c) F1 mice by means of electron microscopy, immunofluorescence and radioautography. The experimental models are murine leucoencephalomyelitis induced by either mouse hepatitis virus (MHV) or DA strain of Theiler's mouse encephalomyelitis virus (DAV). The objectives are to: 1) identify subpopulations of T-lymphocytes in the inflammatory demyelinating lesions at different stages of disease and compare their distribution to lesions produced by allergic encephalomyelitis (EAE). 2) Determine cellular hypersensitivity of spleen cells against mouse spinal cord homogenate (MSCH), myelin basic protein (MBP) and inactivated DAV during the course of DAV induced demyelination. 3) Transfer lymphnode and spleen cells from mice prior to and during the development of white matter lesions after infection with DAV and search for histologic lesions in recipient mice using as positive controls the transfer of lymphoid cells from mice afflicted with EAE. 4) Study remeylination in mice implanted with immunoglobulin producing hybridomas during recovery from MHV infection. The findings are expected to contribute to the understanding of the pathogenesis of human postinfectious encephalomyelitis and multiple sclerosis.