Sriram S, Carroll L
Department of Neurology, University of Vermont, College of Medicine, University Health Center, Burlington 05401.
Cell Immunol. 1991 Jun;135(1):222-31. doi: 10.1016/0008-8749(91)90267-f.
In vivo treatment with anti-IA antibodies has been shown to induce a haplotype-specific inhibition of EAE when the disease was following passive transfer of MBP-sensitized T cells. In order to determine the mechanism by which anti-IA antibody prevents passively transferred EAE, the homing of radiolabeled cells to the brain following anti-IA therapy was studied. Administration of anti-IA antibodies at the earliest onset of clinical signs of EAE prevented the homing of radio-labeled cells to the brain. In F1 (Balb/c x SJL/J) mice that developed EAE and received anti-IAs antibody there was a decreased homing of radiolabeled cells when compared to animals that received anti-IAd antibody. In addition, there was preferential expression of IAs antigen, over IAd antigen on capillary endothelium of the brain. The differential expression of IA antigens and the homing of radiolabeled cells in F1 (SJL x Balb/c) mice could in part explain the haplotype-specific suppression of disease following treatment with anti-IA antibodies.
当疾病是在髓鞘碱性蛋白致敏的T细胞被动转移后发生时，用抗IA抗体进行体内治疗已显示可诱导对实验性自身免疫性脑脊髓炎（EAE）的单倍型特异性抑制。为了确定抗IA抗体预防被动转移的EAE的机制，研究了抗IA治疗后放射性标记细胞向脑内的归巢情况。在EAE临床症状最早出现时给予抗IA抗体可阻止放射性标记细胞向脑内归巢。在发生EAE并接受抗IAs抗体的F1（Balb/c×SJL/J）小鼠中，与接受抗IAd抗体的动物相比，放射性标记细胞的归巢减少。此外，脑毛细血管内皮上IAs抗原的表达优先于IAd抗原。F1（SJL×Balb/c）小鼠中IA抗原的差异表达和放射性标记细胞的归巢可以部分解释抗IA抗体治疗后疾病的单倍型特异性抑制。
