小胶质细胞
免疫学
自分泌信号
多发性硬化
一氧化氮
神经营养因子
白细胞介素
发病机制
医学
神经科学
细胞因子
生物
炎症
受体
内分泌学
内科学
作者
Jun Kawanokuchi,Kiyokazu Shimizu,Atsumi Nitta,Kiyofumi Yamada,Tetsuya Mizuno,Hideyuki Takeuchi,Akio Suzumura
标识
DOI:10.1016/j.jneuroim.2007.11.006
摘要
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-1β. Because microglia produce IL-1β 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.
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