作者: H. Takimoto , H. Maruyama , K.-I. Shimada , R. Yakabe , I. Yano
DOI: 10.1111/J.1365-2249.2006.03043.X
关键词: Lipoarabinomannan 、 Immunology 、 Microbiology 、 Interferon 、 Interferon gamma 、 Tumor necrosis factor alpha 、 Biology 、 Cord factor 、 Trehalose dimycolate 、 Interleukin 、 Alveolar macrophage 、 Immunology and Allergy
摘要: The mechanisms by which pulmonary granuloma formation is caused administration of mycobacterial glycolipids such as trehalose dimycolate (TDM), lipoarabinomannan (LAM) and phosphatidylinositol mannosides (PIM) were investigated. When peritoneal alveolar macrophages stimulated with TDM, LAM PIM in vitro, TDM exhibited the strongest tumour necrosis factor (TNF)-inducing activity. Responsiveness from mice defected Toll-like receptor 4 (TLR4) was much higher than that wild-type mice. Although also had a significant activity, rather TNF-alpha production macrophage. injected water-in-oil-in-water emulsion into via tail vein, development response to related closely their TNF-inducing activity Granuloma observed not only lacking interleukin (IL)-12 signalling but interferon (IFN)-gamma knock-out correlated levels lungs. Administration anti-TNF-alpha monoclonal antibody TDM-injected IFN-gamma decreased formation, suggesting due IFN-gamma-independent TNF-alpha-dependent pathway.