摘要
Glatiramer 醋酸盐(GA ) 是过去常对待多重硬化的 immunomodulatory 肽药。它的处理效果被扩展了到象 uveoretinitis，煽动性的肠疾病，接枝拒绝和肝的纤维变性那样的另外的自体免疫的条件。这里，我们报导 GA 在在 cyclophosphamide (CY ) 改变糖尿病的临床的功课是有效的加强的非肥胖的糖尿病患者(CY 点头) 老鼠。有显著地减少的 GA 的治疗在老鼠和改善 insulitis 的糖尿病的率，它与增加的 CD4+CD25+Foxp3+ T 房间反应与一致在对待老鼠。GA 处理导致了抄写因素 Foxp3 的增加的表示并且在 vivo 并且在 vitro 提高了 interleukin-4 (IL-4 ) 的生产。Foxp3 的起来规定上的 GA 的效果通过 IL-4 部分被调停，是明显的。IL-4 被发现维持 Foxp3 表示和 CD4+CD25+ 规章的 T 房间(Tregs ) 的规章的功能。这研究提供 GA 通过 Tregs 的正式就职为类型 1 糖尿病有处理潜力，那增加的 IL-4 生产为提高的 Treg 在 GA 处理的功能部分负责的新证据。
Glatiramer acetate （GA） is an immunomodulatory peptide drug used to treat multiple sclerosis. Its treatment effect has been expanded to other autoimmune conditions such as uveoretinitis, inflammatory bowel disease, graft re- jection and hepatic fibrosis. Here, we report that GA was effective in altering the clinical course of diabetes in cyclo- phosphamide （CY）-potentiated non-obese diabetic （CY-NOD） mice. Treatment with GA significantly reduced the dia- betic rate in the mice and ameliorated insulitis, which coincided with increased CD4＋CD25＋Foxp3＋ T cell response in treated mice. GA treatment led to increased expression of transcription factor Foxp3 and elevated production of interleukin-4 （IL-4） both in vivo and in vitro. It was evident that the effect of GA on up-regulation of Foxp3 was me- diated partially through IL-4. IL-4 was found to maintain Foxp3 expression and regulatory function of CD4＋CD25＋ regulatory T cells （Tregs）. This study provides new evidence that GA has treatment potential for type 1 diabetes through the induction of Tregs and that increased IL-4 production is partially responsible for the enhanced Treg＇s function in GA treatment.
