Department of Pathological Biochemistry, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
Biol Pharm Bull. 2011;34(6):933-6. doi: 10.1248/bpb.34.933.
FTY720 (Fingolimod) is known to have a significant therapeutic effect on experimental autoimmune encephalomyelitis (EAE). Here, we used an EAE mouse model, which had been established by immunizing C57BL/6J mice with a partial peptide of myelin oligodendrocyte glycoprotein (MOG₃₅₋₅₅), to examine the relapse of EAE upon discontinuation of treatment with FTY720 alone or in combination with MOG₃₅₋₅₅. Relapse was confirmed to occur in all animals (n=6) within one week after discontinuation of FTY720, with increase in the number of lymphocytes infiltrating the spinal cord and demyelination. However, in the case of combination therapy with FTY720 and MOG₃₅₋₅₅, relapse following discontinuation of treatment was completely suppressed. The autoantigenic peptide might serve to suppress the clonal selection of relapse-associated autoantigen-specific T cells.
FTY720（fingolimod）已被证实对实验性自身免疫性脑脊髓炎（EAE）具有显著的治疗作用。在这里，我们使用了一种 EAE 小鼠模型，该模型通过用髓鞘少突胶质细胞糖蛋白（MOG₃₅₋₅₅）的部分肽免疫 C57BL/6J 小鼠来建立，以检查单独使用 FTY720 或与 MOG₃₅₋₅₅联合治疗后 EAE 的复发情况。在停止 FTY720 治疗后一周内，所有动物（n=6）均确认发生复发，脊髓中的淋巴细胞浸润和脱髓鞘增加。然而，在 FTY720 和 MOG₃₅₋₅₅联合治疗的情况下，停药后的复发完全得到抑制。这种自身抗原肽可能抑制与复发相关的自身抗原特异性 T 细胞的克隆选择。
