Department of Dermatology, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, China.
Department of Central Laboratory, First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian 350005, China.
J Neuroimmunol. 2014 Apr 15;269(1-2):9-19. doi: 10.1016/j.jneuroim.2014.01.010. Epub 2014 Jan 30.
Alpha-melanocyte stimulating hormone (α-MSH) plays a crucial role in the regulation of immune and inflammatory reactions. Here we report that SVα-MSH, a novel α-MSH analog, could ameliorate the clinical severity of experimental autoimmune encephalomyelitis (EAE) in a preventive and therapeutic manner. SVα-MSH treatment induced the production of regulatory T (Treg) cells and reduced the Th17 cells in the CNS of EAE mice. SVα-MSH-treated PLP peptide 139-151-specific T cells showed a down-regulation of T cell activation markers CD69 and CD134. SVα-MSH did not induce apoptosis but blocked the G1/S phase transition, reduced the expression of cyclin E, Cdk2 and the activity of NFAT and AP-1 transcription factors. Thus, SVα-MSH acts as a novel immunotherapeutic approach in the treatment of autoimmune attack on the CNS.
α-黑色素细胞刺激素（α-MSH）在调节免疫和炎症反应中起着至关重要的作用。在这里，我们报告说，SVα-MSH，一种新型的α-MSH 类似物，可以通过预防和治疗的方式改善实验性自身免疫性脑脊髓炎（EAE）的临床严重程度。SVα-MSH 治疗诱导了调节性 T（Treg）细胞的产生，并减少了 EAE 小鼠中枢神经系统中的 Th17 细胞。SVα-MSH 处理的 PLP 肽 139-151 特异性 T 细胞显示 T 细胞活化标志物 CD69 和 CD134 的下调。SVα-MSH 没有诱导细胞凋亡，但阻断了 G1/S 期转变，降低了细胞周期蛋白 E、Cdk2 的表达以及 NFAT 和 AP-1 转录因子的活性。因此，SVα-MSH 可作为治疗中枢神经系统自身免疫攻击的一种新的免疫治疗方法。
