Lafaille J J, Nagashima K, Katsuki M, Tonegawa S
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Cell. 1994 Aug 12;78(3):399-408. doi: 10.1016/0092-8674(94)90419-7.
We have generated TCR transgenic mice (T/R+) specific for myelin basic protein (MBP) and crossed them to RAG-1-deficient mice to obtain mice (T/R-) that have T cells expressing the transgenic TCR but no other lymphocytes. Both T/R+ and T/R- mice carry, in the lymph nodes and spleen, large numbers of the potentially encephalitogenic CD4+ anti-MBP T cells. These cells respond to MBP in vitro but show no signs of activation in vivo. Nevertheless, approximately 14% of H-2u T/R+ and 100% of H-2u T/R- mice developed spontaneous experimental autoimmune encephalomyelitis (EAE) within 12 months. These data indicate that EAE can be mediated by CD4+ anti-MBP T cells in the absence of any other lymphocytes and that nontransgenic lymphocytes that are present in T/R+ but absent in T/R- mice have a protective effect. The data also suggest that spontaneous EAE may be triggered by an in situ activation of CD4+ anti-MBP cells in the nervous system.
我们构建了针对髓鞘碱性蛋白(MBP)的T细胞受体转基因小鼠(T/R+),并将它们与RAG-1缺陷小鼠杂交,以获得具有表达转基因T细胞受体但无其他淋巴细胞的小鼠(T/R-)。T/R+和T/R-小鼠在淋巴结和脾脏中都携带大量潜在致脑炎性的CD4+抗MBP T细胞。这些细胞在体外对MBP有反应,但在体内未表现出激活迹象。然而,大约14%的H-2u T/R+小鼠和100%的H-2u T/R-小鼠在12个月内发生了自发性实验性自身免疫性脑脊髓炎(EAE)。这些数据表明,EAE可由CD4+抗MBP T细胞在无任何其他淋巴细胞的情况下介导,并且T/R+小鼠中存在而T/R-小鼠中不存在的非转基因淋巴细胞具有保护作用。数据还表明,自发性EAE可能由神经系统中CD4+抗MBP细胞的原位激活引发。