Jungi T W, Brcic M, Leutwyler C, Pfister H, Spycher M O
Institute of Veterinary Virology, University of Berne, Switzerland.
Immunology. 1991 Nov;74(3):439-45.
The influence of priming by interferon-gamma (IFN-gamma) on FcR expression and function was investigated with human monocyte-derived macrophages. As a ligand specifically interacting with FcRII, bovine IgG1-coated erythrocytes (Bo1-EA) were used. The uptake of these particles by human monocytes and macrophages could be inhibited with anti-FcRII. Moreover, macrophages representing the phenotype that fails to interact with murine IgG1, as revealed in an anti-CD3 IgG1-driven T-cell proliferation assay, had a low avidity for Bo1-EA, and Bo1-EA-macrophage interaction could not be inhibited by anti-FcRII in these cells. Thus, anti-Leu-4 non-responsiveness in a T-cell stimulation assay is associated with an inability of FcRII to interact with bovine IgG1. An influence of IFN-gamma priming on FcRII expression and function was studied, therefore, in anti-Leu-4 responders (bovine IgG1 high responders in the phagocytosis test, susceptible to anti-FcRII treatment). IFN-gamma-primed macrophages from such donors displayed a markedly reduced phagocytosis of Bo1-EA. This reduction was observed both with adherent and with suspended macrophages This type of modulation was not due to a reduced expression of FcRII, nor due to a reduced avidity of expressed FcR to its ligand, as revealed by flow cytometric and rosetting analysis. Since phagocytosis of latex particles and of tanned erythrocytes is little influenced by IFN-gamma priming, our data suggest that IFN-gamma affects FcRII-mediated phagocytosis by a post-receptor-binding mechanism.
利用人单核细胞衍生的巨噬细胞研究了γ-干扰素（IFN-γ）引发对FcR表达和功能的影响。作为与FcRII特异性相互作用的配体，使用了包被牛IgG1的红细胞（Bo1-EA）。人单核细胞和巨噬细胞对这些颗粒的摄取可被抗FcRII抑制。此外，在抗CD3 IgG1驱动的T细胞增殖试验中显示，代表不能与鼠IgG1相互作用表型的巨噬细胞对Bo1-EA的亲和力较低，并且在这些细胞中抗FcRII不能抑制Bo1-EA与巨噬细胞的相互作用。因此，T细胞刺激试验中的抗Leu-4无反应性与FcRII不能与牛IgG1相互作用有关。因此，在抗Leu-4反应者（吞噬试验中对牛IgG1高反应，易受抗FcRII处理影响）中研究了IFN-γ引发对FcRII表达和功能的影响。来自此类供体的经IFN-γ引发的巨噬细胞对Bo1-EA的吞噬作用明显降低。无论是贴壁巨噬细胞还是悬浮巨噬细胞均观察到这种降低。流式细胞术和玫瑰花结分析显示，这种调节类型不是由于FcRII表达降低，也不是由于表达的FcR对其配体的亲和力降低。由于乳胶颗粒和鞣酸红细胞的吞噬作用受IFN-γ引发的影响很小，我们的数据表明IFN-γ通过受体后结合机制影响FcRII介导的吞噬作用。
