Kawanokuchi Jun, Shimizu Kouki, Nitta Atsumi, Yamada Kiyofumi, Mizuno Tetsuya, Takeuchi Hideyuki, Suzumura Akio
Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan.
J Neuroimmunol. 2008 Feb;194(1-2):54-61. doi: 10.1016/j.jneuroim.2007.11.006. Epub 2007 Dec 31.
Interleukin (IL)-17-producing helper T cells may play a pivotal role in the pathogenesis of multiple sclerosis. Here, we examined the effects of IL-17 on microglia, which are known to be critically involved in multiple sclerosis. Treatment with IL-17 upregulated the microglial production of IL-6, macrophage inflammatory protein-2, nitric oxide, adhesion molecules, and neurotrophic factors. We also found that IL-17 was produced by microglia in response to IL-23 or IL-1beta. Because microglia produce IL-1beta and IL-23, these cytokines may act in an autocrine manner to induce IL-17 expression in microglia, and thereby contribute to autoimmune diseases, such as MS, in the central nervous system.
产生白细胞介素(IL)-17的辅助性T细胞可能在多发性硬化症的发病机制中起关键作用。在此,我们研究了IL-17对小胶质细胞的影响,已知小胶质细胞在多发性硬化症中起关键作用。用IL-17处理可上调小胶质细胞中IL-6、巨噬细胞炎性蛋白-2、一氧化氮、黏附分子和神经营养因子的产生。我们还发现,小胶质细胞在对IL-23或IL-1β的反应中产生IL-17。由于小胶质细胞产生IL-1β和IL-23,这些细胞因子可能以自分泌方式作用,诱导小胶质细胞中IL-17的表达,从而促进中枢神经系统中的自身免疫性疾病,如多发性硬化症。