Guyre P M, Morganelli P M, Miller R
J Clin Invest. 1983 Jul;72(1):393-7. doi: 10.1172/jci110980.
Although recent studies suggest that interferons can increase the number of IgG Fc receptor (FcR gamma) sites on mouse macrophages, direct assessment of similar effects on human mononuclear phagocytes is lacking. We therefore measured the specific binding of 125I- and fluorescein-labeled IgG1 to human monocytes and leukemic cell lines after culture in vitro with highly purified human interferons. We report that natural and recombinant human gamma-interferon causes a dramatic (nearly 10-fold) increase in the number of FcR gamma on normal human monocytes and on the human cell lines HL-60 and U-937. Alpha and beta-interferons cause a modest but significant increase in these receptors. This report demonstrates that gamma-interferon acts directly on human mononuclear phagocytes to increase FcR gamma sites, it identifies a qualitative difference in the physiologic actions of human type I and type II interferons, and it suggests that HL-60 and U-937 cells will be important models for further study of the molecular mechanisms of interferon action. The results reported here could also be the basis for a bioassay to assess the pharmacokinetics and variability of gamma-interferon action on monocytes of individual patients during treatment in vitro and in vivo.
尽管最近的研究表明，干扰素可增加小鼠巨噬细胞上IgG Fc受体（FcRγ）位点的数量，但缺乏对人类单核吞噬细胞类似作用的直接评估。因此，我们在用高度纯化的人类干扰素体外培养后，测量了125I和荧光素标记的IgG1与人类单核细胞和白血病细胞系的特异性结合。我们报告，天然和重组人类γ干扰素可使正常人单核细胞以及人类细胞系HL-60和U-937上的FcRγ数量显著增加（近10倍）。α和β干扰素可使这些受体数量适度但显著增加。本报告表明，γ干扰素直接作用于人类单核吞噬细胞以增加FcRγ位点，它确定了人类I型和II型干扰素生理作用的质的差异，并且表明HL-60和U-937细胞将成为进一步研究干扰素作用分子机制的重要模型。此处报告的结果也可能成为一种生物测定法的基础，以评估γ干扰素在体外和体内治疗期间对个体患者单核细胞作用的药代动力学和变异性。
