Alford P B, Xue Y, Shackelford R E
Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA.
Biochem Biophys Res Commun. 1997 Nov 17;240(2):442-5. doi: 10.1006/bbrc.1997.7670.
The macrophage-colony stimulating factor receptor, c-fms, is induced by IL-2 in monocytes and is suppressed by LPS, LPS plus IFN-gamma, phorbol esters, and colony stimulating factor in monocytes/macrophages. Here we show that c-fms RNA is induced by treatment of murine tissue macrophages with TNF-alpha. This induction is suppressed by co-treatment with LPS, IFN-gamma, LPS plus IFN-gamma, aspirin, and ox LDL. c-fms expression is required for the proliferation, differentiation, and survival of monocytes/macrophages. Our findings indicate a way by which TNF-alpha, as well as LPS, IFN-gamma, aspirin, and ox LDL impinge upon macrophage biology.
巨噬细胞集落刺激因子受体c-fms，在单核细胞中由白细胞介素-2诱导产生，而在单核细胞/巨噬细胞中则被脂多糖、脂多糖加干扰素-γ、佛波酯和集落刺激因子所抑制。在此我们表明，用肿瘤坏死因子-α处理小鼠组织巨噬细胞可诱导c-fms RNA的产生。脂多糖、干扰素-γ、脂多糖加干扰素-γ、阿司匹林和氧化型低密度脂蛋白共同处理可抑制这种诱导作用。单核细胞/巨噬细胞的增殖、分化和存活需要c-fms的表达。我们的研究结果揭示了肿瘤坏死因子-α以及脂多糖、干扰素-γ、阿司匹林和氧化型低密度脂蛋白影响巨噬细胞生物学特性的一种方式。
