Fischer T, Wiegmann K, Böttinger H, Morens K, Burmester G, Pfizenmaier K
Klinische Arbeitsgruppe der Max-Planck-Gesellschaft, University of Göttingen, F.R.G.
J Immunol. 1990 Nov 1;145(9):2914-9.
The regulation of human IFN-gamma receptor (IFN-gamma-R) expression by granulocyte-macrophage CSF (GM-CSF) was investigated. On monocytic cell lines (U937, HL60) and peripheral blood monocytes, IFN-gamma-binding capacity was down-regulated upon incubation with GM-CSF. Scatchard plot analyses revealed that down-regulation was caused by a decrease in IFN-gamma-R number rather than by a change in affinity. GM-CSF treatment did not reduce IFN-gamma-R-specific mRNA levels, but reduced the half-life of membrane-expressed IFN-gamma-R, indicating a post-translational control of IFN-gamma-R by GM-CSF. Because both IFN-gamma and GM-CSF are crucially involved in activation of monocytic function, the data presented suggest that down-regulation of IFN-gamma-R by GM-CSF may represent a potential negative feedback control of monocyte activation. Further studies of IFN-gamma binding characteristics and isolation of IFN-gamma-R by immunoprecipitation revealed that IFN-gamma binding to human peripheral blood monocytes is mediated by a receptor protein structurally and functionally identical to that previously characterized in several established cell lines of other tissue origin.
研究了粒细胞巨噬细胞集落刺激因子（GM-CSF）对人γ干扰素受体（IFN-γ-R）表达的调节作用。在单核细胞系（U937、HL60）和外周血单核细胞上，与GM-CSF孵育后，IFN-γ结合能力下调。Scatchard图分析显示，下调是由IFN-γ-R数量减少引起的，而非亲和力改变所致。GM-CSF处理并未降低IFN-γ-R特异性mRNA水平，但缩短了膜表达IFN-γ-R的半衰期，表明GM-CSF对IFN-γ-R存在翻译后调控。由于IFN-γ和GM-CSF都在单核细胞功能激活中起关键作用，所呈现的数据表明GM-CSF对IFN-γ-R的下调可能代表单核细胞激活的一种潜在负反馈调控。对IFN-γ结合特性的进一步研究以及通过免疫沉淀分离IFN-γ-R表明，IFN-γ与人外周血单核细胞的结合是由一种受体蛋白介导的，该受体蛋白在结构和功能上与先前在其他组织来源的几种既定细胞系中所鉴定的受体蛋白相同。
