Gerhauser Ingo, Alldinger Susanne, Baumgärtner Wolfgang
Department of Pathology, University of Veterinary Medicine Hannover, Hannover, Germany.
J Neuroimmunol. 2007 Aug;188(1-2):86-94. doi: 10.1016/j.jneuroim.2007.05.019. Epub 2007 Jun 27.
Demyelination of Theiler's murine encephalomyelitis (TME) depends on viral persistence and on the mouse genotype. Ets-1 expression, a transcription factor involved in T cell activation and cytokine expression, was investigated in the spinal cord during TME using RT-qPCR and immunohistochemistry. Resistant C57BL/6 mice lacking virus persistence and demyelination demonstrated a stronger upregulation of Ets-1 mRNA transcripts in the early phase of TME compared to susceptible SJL/J mice probably linked to viral clearance. Though strong Ets-1 expression in resident glial cells such as astrocytes might inhibit lesion development, delayed Ets-1 activation in inflammatory cells seemed to promote demyelination in the late phase of TME in SJL/J mice.
泰勒氏鼠脑脊髓炎(TME)的脱髓鞘取决于病毒持续性和小鼠基因型。使用逆转录定量聚合酶链反应(RT-qPCR)和免疫组织化学方法,对TME期间脊髓中参与T细胞活化和细胞因子表达的转录因子Ets-1的表达进行了研究。缺乏病毒持续性和脱髓鞘的抗性C57BL/6小鼠与易感的SJL/J小鼠相比,在TME早期显示出更强的Ets-1 mRNA转录本上调,这可能与病毒清除有关。尽管驻留神经胶质细胞(如星形胶质细胞)中强烈的Ets-1表达可能抑制病变发展,但炎症细胞中Ets-1的延迟激活似乎在SJL/J小鼠TME后期促进了脱髓鞘。