Capsoni F, Minonzio F, Ongari A M, Bonara P, Pinto G, Carbonelli V, Lazzarin A, Zanussi C
Institute of Internal Medicine, Infectious Diseases and Immunopathology, University of Milan, Italy.
Scand J Immunol. 1994 Jan;39(1):45-50. doi: 10.1111/j.1365-3083.1994.tb03338.x.
Fc-receptor (FcR)-mediated phagocytosis and FcR (FcRI, FcRII and FcRIII) membrane expression was studied on freshly separated and cultured monocytes (Mo) from 20 AIDS patients and 20 healthy controls. Both Mo and Mo-derived macrophages from AIDS patients presented a significant defect in their capacity to ingest IgG-coated erythrocytes (EA) compared to control cells. This functional defect did not depend on a decline in the number of FcR+ cells or on a decrease in the expression of FcR on their surface. In fact, the percentages of phagocytes reacting with anti-FcRI MoAb (32.2) or anti-FcRII MoAb (IV.3) were similar for controls and AIDS patients, while the percentage of FcRIII-positive Mo (MoAb 3G8) was higher in the AIDS population than in controls, though this difference was not seen on cultured Mo. The level of FcRI expression, evaluated as mean fluorescence intensity (MFI), was higher on freshly separated Mo from AIDS patients than from controls but this difference disappeared also with differentiation of Mo to Mo-derived macrophages in vitro. Parallel analysis of FcRII and FcRIII on phagocytes revealed no differences in the MFI between the AIDS and control groups. Some observations suggested that this functional defect might be secondary to phagocyte priming by circulating IFN-gamma: (1) in vitro stimulation of Mo with hrIFN-gamma, which increased FcRI expression, actually reduced phagocytosis of IgG-coated particles; and (2) IFN-gamma concentrations were increased in AIDS patients' plasma. In spite of these findings, no significant correlation was found between plasma IFN-gamma concentrations and FcR-mediated ingestion in AIDS patients, making the hypothesis uncertain. Even if the basis for the impaired FcR-mediated phagocytosis in AIDS patients remains unclear, this functional defect may have a role in the immunopathogenesis of AIDS, constituting a component cause of the immunodeficiency.
对20例艾滋病患者和20名健康对照者新鲜分离及培养的单核细胞（Mo）进行了Fc受体（FcR）介导的吞噬作用及FcR（FcRI、FcRII和FcRIII）膜表达的研究。与对照细胞相比，艾滋病患者的Mo及Mo衍生的巨噬细胞摄取IgG包被红细胞（EA）的能力存在显著缺陷。这种功能缺陷并不取决于FcR⁺细胞数量的减少或其表面FcR表达的降低。事实上，对照者和艾滋病患者中与抗FcRI单克隆抗体（32.2）或抗FcRII单克隆抗体（IV.3）反应的吞噬细胞百分比相似，而艾滋病患者中FcRIII阳性Mo（单克隆抗体3G8）的百分比高于对照者，不过在培养的Mo上未观察到这种差异。以平均荧光强度（MFI）评估的FcRI表达水平，在艾滋病患者新鲜分离的Mo上高于对照者，但随着Mo在体外分化为Mo衍生的巨噬细胞，这种差异也消失了。对吞噬细胞上FcRII和FcRIII的平行分析显示，艾滋病组和对照组之间MFI无差异。一些观察结果提示，这种功能缺陷可能继发于循环中的干扰素-γ对吞噬细胞的启动作用：（1）用人重组干扰素-γ（hrIFN-γ）体外刺激Mo，虽增加了FcRI表达，但实际上降低了IgG包被颗粒的吞噬作用；（2）艾滋病患者血浆中干扰素-γ浓度升高。尽管有这些发现，但在艾滋病患者中未发现血浆干扰素-γ浓度与FcR介导的摄取之间存在显著相关性，这使得该假说尚不确定。即使艾滋病患者中FcR介导的吞噬作用受损的原因仍不清楚，但这种功能缺陷可能在艾滋病的免疫发病机制中起作用，构成免疫缺陷的一个组成原因。
