髓鞘少突胶质细胞诱导实验性自身免疫性脑脊髓炎小鼠的中枢病理损伤与Th1、Th17细胞分泌炎症细胞因子的变化观察  

Study of Pathological Injury and Inflammatory Cytokines Produced by Th1,Th17 Cells on MOG-induced Model of Experimental Autoimmune Encephalomyelitis

作　　者：姚苏琴[1] 郑荣远[1,2] 郦铮铮[1] 李晓莉[1,2] 朱英标[1] 童巧文[1] 陈国钱[1,2] 陈江帆[2] 

机构地区：[1]温州医学院附属第一医院神经内科 [2]温州医学院实验神经生物学研究所,325000

出　　处：《中国临床神经科学》2009年第4期351-356,共6页Chinese Journal of Clinical Neurosciences

基　　金：省部共建基金(wzj:2005-2-041)

摘　　要：目的:观察实验性自身免疫性脑脊髓炎(EAE)的中枢神经系统(CNS)病理损伤与Th1、Th17细胞分泌的相关炎症细胞因子的变化,探讨EAE致病的分子免疫学机制。方法:用髓鞘少突胶质细胞(MOG35-55)免疫诱导野生型C57BL/6小鼠制作EAE模型,记录小鼠行为学变化,苏木精-伊红染色观察CNS病理损害,RT-PCR法检测中枢Th1细胞因子γ-干扰素(IFN-γ)、Th17细胞因子IL-17和IL-6的mRNA表达水平。结果:MOG诱导的EAE模型组小鼠出现典型的EAE行为及病理学表现,大脑组织中INF-γ、IL-17和IL-6mRNA表达水平均较CFA对照组有明显升高。结论:在EAE炎症反应的过程中,Th1细胞和Th17细胞激活,各自分泌的炎症细胞因子(INF-γ、IL-6、IL-17)增加,它们可能参与了EAE发病的重要免疫病理机制。EAE的致病并不是单一Th1或者Th17细胞作用的结果,而是两类细胞因子都参与了作用。Aim： To observe the behavioral and histological changes as well as the expression of Thl and Th17 cell cytokines in mouse brain and cervical cord in EAE, and to explore the molecular immunological mechanism in the model. Methods： MOG35-55 were used to establish EAE model on C57BL/6 mice. The behavioral changes and the histological scores were recorded and examined. Meanwhile the expressions of Th 1 cytokine INF-γ, Th 17 cytokine IL-17 and IL-6 mRNA in brain were detected with reverse transcription polymerase chain reaction （RT-PCR）. Results： It was shown that the model mice developed a typical clinical and histological EAE manifestation. In addition, a marked increase in gene expression of INF-γ, IL-17 and IL- 6 was detected in the brain tissue of the mice from the EAE model compared with CFA control group. Conclusion： In EAE inflammatory process, the activation of Th1 and Th17 cells and the increase of cytokines secreted by these cells are important immunopathological contributors resulting in the incidence of EAE.

关 键 词：实验性自身免疫性脑脊髓炎 辅助性T细胞 γ-干扰素 白介素17 白介素6 

分 类 号：R744.53[医药卫生—神经病学与精神病学]