一种针对表达对髓鞘少突胶质细胞糖蛋白具有特异性的转基因TCR的小鼠实验性变应性脑脊髓炎的新型保护模型。
A novel protective model against experimental allergic encephalomyelitis in mice expressing a transgenic TCR-specific for myelin oligodendrocyte glycoprotein.
作者信息
Mendel Itzhak, Natarajan Kannan, Ben-Nun Avraham, Shevach Ethan M
机构信息
Laboratory of Immunology, Cellular Immunology Section, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N315, 10 Center Drive, Bethesda, MD 20892-1892, USA.
出版信息
J Neuroimmunol. 2004 Apr;149(1-2):10-21. doi: 10.1016/j.jneuroim.2003.12.007.
Myelin oligodendrocyte glycoprotein (MOG) is an important autoantigen in multiple sclerosis and in experimental autoimmune encephalomyelitis (EAE). We generated a T cell receptor (TCR) transgenic (Tg) mouse expressing a TCR derived from an encephalitogenic T cell clone specific for MOG(35-55). This mouse failed to develop EAE spontaneously and developed mild EAE at late onset when immunized with MOG(35-55). The Tg T cells produced large amounts of IL-4 when stimulated with MOG(35-55) and underwent FAS/FAS-L-mediated activation-induced cell death when stimulated with MOG(35-55) and IL-12. The unique phenotype of these autoantigen-specific T cells may represent an important mechanism of protection against autoimmune disease.
髓鞘少突胶质细胞糖蛋白（MOG）是多发性硬化症和实验性自身免疫性脑脊髓炎（EAE）中的一种重要自身抗原。我们构建了一种T细胞受体（TCR）转基因（Tg）小鼠，其表达源自对MOG（35-55）特异的致脑炎性T细胞克隆的TCR。该小鼠不能自发发生EAE，在用MOG（35-55）免疫时，在晚期发生轻度EAE。当用MOG（35-55）刺激时，Tg T细胞产生大量IL-4，当用MOG（35-55）和IL-12刺激时，经历FAS/FAS-L介导的活化诱导的细胞死亡。这些自身抗原特异性T细胞的独特表型可能代表了预防自身免疫性疾病的一种重要机制。
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