Gammaglobulin for intravenous use induces an Fc gamma receptor-specific decrement in phagocytosis by blood monocytes.

Overview

Intravenous gammaglobulin (IVIG) increases the circulating platelet count in patients with idiopathic thrombocytopenic purpura in association with mononuclear phagocyte system blockade and decreased blood monocyte phagocytosis. To investigate whether IVIG treatment induces an Fc receptor-specific defect or a generalized phagocytic dysfunction which might impair host defenses, we studied the influence of IVIG on Fc receptor-dependent and Fc receptor-independent internalization by monocytes. In purified monocytes incubated in suspension with IVIG (10 mg IgG/ml) for 48 hr, our data demonstrate that Fc receptor-mediated phagocytosis of IgG-sensitized erythrocytes (EA) is significantly decreased. By contrast, there was no significant change in the phagocytosis of neuraminidase-treated erythrocytes which are internalized via the B-glucan receptor. A similar decrease in EA ingestion was observed in adherent monocytes incubated with IVIG. By contrast, the capacity of IVIG-treated adherent monocytes to internalize tannic acid-treated erythrocytes, an Fc receptor-independent probe, was the same as that of control cells. These findings demonstrate that IVIG does not induce a generalized phagocytic blockade, but rather a selective deficit in Fc gamma receptor-mediated internalization. Thus, Fc receptor-independent mechanisms may provide adequate mononuclear phagocyte system function for host defense in patients receiving IVIG.