Flügel A, Berkowicz T, Ritter T, Labeur M, Jenne D E, Li Z, Ellwart J W, Willem M, Lassmann H, Wekerle H
Max-Planck-Institute of Neurobiology, Department of Neuroimmunology, 82152 Martinsried, 10098, Berlin, Germany.
Immunity. 2001 May;14(5):547-60. doi: 10.1016/s1074-7613(01)00143-1.
Homing behavior and function of autoimmune CD4+ T cells in vivo was analyzed before and during EAE, using MBP-specific T cells retrovirally engineered to express the gene of green fluorescent protein. The cells migrate from parathymic lymph nodes to blood and to the spleen. Preceding disease onset, large numbers of effector cells invade the CNS, with only negligible numbers left in the periphery. In early EAE, most (>90%) infiltrating CD4+ cells were effector cells. Migratory effector cells downregulate activation markers (CD25, OX-40) but upregulate several chemokine receptors and adsorb MHC class II on their membranes. Within the CNS, the effector cells are reactivated, with upregulated proinflammatory cytokines and downmodulated T cell receptor-associated structures, presumably reflecting autoantigen recognition in situ.
利用经逆转录病毒工程改造以表达绿色荧光蛋白基因的髓鞘碱性蛋白特异性T细胞,在实验性自身免疫性脑脊髓炎(EAE)之前及发病过程中分析了自身免疫性CD4 + T细胞在体内的归巢行为和功能。这些细胞从胸腺旁淋巴结迁移至血液和脾脏。在疾病发作之前,大量效应细胞侵入中枢神经系统(CNS),外周仅残留数量可忽略不计的细胞。在早期EAE中,大多数(> 90%)浸润的CD4 +细胞是效应细胞。迁移性效应细胞下调激活标志物(CD25、OX-40),但上调几种趋化因子受体,并在其细胞膜上吸附II类主要组织相容性复合体(MHC)。在CNS内,效应细胞被重新激活,促炎细胞因子上调,T细胞受体相关结构下调,这大概反映了原位自身抗原识别。