Wang G-Y, Sun B, Kong Q-F, Zhang Y, Li R, Wang J-H, Wang D-D, Lv G X, Li H-L
Department of Neurobiology, Harbin Medical University Provincial Key Lad of Neurobiology, Harbin, Heilongjiang, China.
Scand J Immunol. 2008 Dec;68(6):589-97. doi: 10.1111/j.1365-3083.2008.02174.x.
Interleukin (IL)-17 is a proinflammatory cytokine primarily secreted by Th17 cells, which are a CD4(+) T-cell subset. Th17 cells and IL-17 are important in the pathogenesis of multiple sclerosis and in its established animal model, experimental autoimmune encephalomyelitis (EAE). However, it is unclear whether IL-17 contributes to EAE immune tolerance. We used the myelin basic protein (MBP) peptide MBP 68-86 to induce nasal tolerance to EAE, and simultaneously interfered with the tolerance by treatment with different doses of IL-17. We found that IL-17 dramatically interfered with MBP 68-86-induced immune tolerance. IL-17 administration increased IL-6 release, skewing T cell differentiation towards Th17 cells and decreasing the number of Treg cells. This led to an imbalance between Treg cells and Th17 cells and spurred the development of EAE.
白细胞介素（IL）-17是一种主要由Th17细胞分泌的促炎细胞因子，Th17细胞是CD4(+) T细胞亚群。Th17细胞和IL-17在多发性硬化症及其成熟的动物模型实验性自身免疫性脑脊髓炎（EAE）的发病机制中起重要作用。然而，尚不清楚IL-17是否有助于EAE免疫耐受。我们使用髓鞘碱性蛋白（MBP）肽MBP 68-86诱导对EAE的鼻内耐受，并同时用不同剂量的IL-17处理来干扰这种耐受。我们发现IL-17显著干扰了MBP 68-86诱导的免疫耐受。给予IL-17会增加IL-6释放，使T细胞分化偏向Th17细胞，并减少调节性T细胞（Treg细胞）的数量。这导致Treg细胞与Th17细胞之间失衡，并促进了EAE的发展。
