针对髓鞘少突胶质细胞糖蛋白（MOG）的记忆细胞可控制实验性自身免疫性脑脊髓炎的转移。
Memory cells specific for myelin oligodendrocyte glycoprotein (MOG) govern the transfer of experimental autoimmune encephalomyelitis.
机构信息
The Ohio State University, Department of Molecular Virology, Immunology, and Medical Genetics, 760 Biomedical Research Tower, 460 W 12th Avenue, Columbus, OH 43210, USA.
出版信息
J Neuroimmunol. 2011 May;234(1-2):84-92. doi: 10.1016/j.jneuroim.2011.02.008. Epub 2011 Apr 3.
Abstract
Multiple sclerosis (MS) is an inflammatory disease of the CNS mediated by CD4(+) T cells directed against myelin antigens. Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with myelin antigens like myelin oligodendrocyte glycoprotein (MOG). We have explored the transfer of EAE using MOG(35-55)-specific TCR transgenic (2D2) T cells. Unsorted 2D2 Th1 cells reliably transferred EAE. Further, we found that CD44(hi)CD62L(lo) effector/memory CD4(+) T cells are likely responsible for the disease transfer due to the up-regulation of CD44. Given the importance of MOG in MS pathogenesis, mechanistic insights into adoptively transferred EAE by MOG-specific Th1 cells could prove valuable in MS research.
摘要
多发性硬化症（MS）是一种由中枢神经系统炎症引起的疾病，其介导物是针对髓鞘抗原的 CD4(+)T 细胞。实验性自身免疫性脑脊髓炎（EAE）是通过用髓鞘抗原如髓鞘少突胶质细胞糖蛋白（MOG）免疫诱导产生的。我们使用髓鞘寡糖蛋白（MOG）（35-55）特异性 TCR 转基因（2D2）T 细胞探索了 EAE 的转移。未分选的 2D2Th1 细胞可靠地转移了 EAE。此外，我们发现由于 CD44 的上调，CD44(hi)CD62L(lo)效应/记忆 CD4(+)T 细胞可能是导致疾病转移的原因。鉴于 MOG 在 MS 发病机制中的重要性，通过 MOG 特异性 Th1 细胞进行的过继转移 EAE 的机制见解可能对 MS 研究具有重要价值。
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