EAE小鼠模型的构建及其免疫学机制的探讨  

Establishment of murine experimental autoimmune encephalomyelitis model and study of the immunologic mechanisms

作　　者：泰淑红[1] 李虹[2] 贾静[3] 吕梅励[1] 张林[3] 

机构地区：[1]四川大学华西基础医学与法医学院免疫教研室 ,成都610041 [2]四川大学华西基础医学与法医学院微生物教研室,成都610041 [3]四川大学基础医学与法医学院物证教研室,成都610041

出　　处：《免疫学杂志》2008年第1期34-37,共4页Immunological Journal

基　　金：中华纽约基金会(CMB)项目(88-486);四川省应用基础项目(04JY029-002)资助

摘　　要：目的用髓鞘少突胶质细胞糖蛋白35-55(MOG35-55)多肽免疫C57BL/6小鼠建立实验性自身免疫性脑脊髓炎(EAE)模型并初步探讨EAE发病的免疫学机制。方法用MOG35-55抗原免疫C57BL/6小鼠,观察实验动物的症状及中枢神经系统的病理改变;应用MTT法测定EAE小鼠脾脏T淋巴细胞活化增殖程度;应用ELISA技术测定EAE小鼠血清IFN-γ浓度和抗MOG35-55抗体水平。结果EAE组发病率为100%,HE染色观察到脑脊髓炎性细胞浸润,白质脱髓鞘等病理改变;EAE小鼠脾脏MOG35-55反应性T淋巴细胞增殖活化,血清IFN-γ浓度和抗MOG35-55抗体随病情的加重而升高。结论用MOG35-55多肽成功诱导了C57BL/6小鼠EAE模型;并推断EAE的发生可能与MOG35-55反应性T淋巴细胞的活化、抗MOG35-55抗体和IFN-γ升高有关。Objective To establish experimental autoimmune encephalomyelitis （EAE） models of C57BL/6 mice induced by Myelin oligodendroeyte glycoprotein （MOG）35-55 and explore the immtmologic mechanisms of EAE. Methods The clinical symptoms and histopathologic changes in the central nervous system （CNS） of C57BL/6 mice immunized with MOG35-55 peptide were observed. Responses of splenic T lymphocytes to MOG35-55 were detected by methods of MTr; the serum anti-MOG35-55 antibodies levels and the serum interferon-γ （IFN-γ） coneentrations were detected by methods of ELISA. Results The EAE group developed the typical symptoms of EAE with the incidence of 100% ; the infiltration of inflammatory cells in brains and spinal cords and the demyelination of the white matter were observed through HE staining. There was an active T cell proliferation to MOG35-55, a marked IFN-γ increase and anti-MOG35-55 antibody increase which paralleled with clinical severity in EAE group. Conclusion EAE models of C57BL/6 mice induced by MOG35-55 have been established successfully in the present study. The activity of T cell response to MOG35-55 and the increases of anti-MOG35-55 antibody and IFN-γ levels may play key roles in the onset of EAE.

关 键 词：髓鞘少突胶质细胞糖蛋白 实验性自身免疫性脑脊髓炎 干扰素-Γ 

分 类 号：R-332[医药卫生] R392