促炎细胞因子
外周血单个核细胞
免疫系统
神经节苷脂
发病机制
免疫学
肿瘤坏死因子α
炎症
生物
细胞培养
细胞因子
坏死
医学
T细胞
细胞
中枢神经系统
小胶质细胞
化学
细胞免疫
背景(考古学)
外围设备
免疫
白细胞介素
作者
Kotaro Mizutani,Nobuyuki Oka,Ichiro Akiguchi,Hitoshi Satoi,Teruaki Kawasaki,Ryuji Kaji,Jun Kimura
出处
期刊:Neuroreport
[Lippincott Williams & Wilkins]
日期:1999-03-01
卷期号:10 (4): 703-706
被引量:12
标识
DOI:10.1097/00001756-199903170-00008
摘要
Some gangliosides have been regarded as autoantigens of immune-mediated neurological disorders such as Guillain-Barré syndrome (GBS), Miller Fisher syndrome and multifocal motor neuropathy. On the other hand, proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), may be important in the pathogenesis of some neuroimmunological disorders. To clarify the interactions between immune cells and gangliosides, we investigated the effects of gangliosides on the production of proinflammatory cytokines in peripheral blood mononuclear cell (PBMC) cultures. We found that ganglioside GM2 markedly enhances the production of TNF-alpha and that TNF-alpha induction by coated GM2 is still more marked. These findings suggest that immune cells, especially monocytes/macrophages, cause inflammation upon encountering GM2.
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