Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule.

C3H/HeJ mice possess macrophages that lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) when cultured. This defect in Fc receptor capacity is completely overcome by treatment of macrophage monolayers with extremely low concentrations of a lymphokine-rich, Con A-stimulated spleen cells supernatant. In this study we have pursued a biochemical and functional analysis of the lymphokine-rich supernatant to determine the nature of the specific factor responsible for the restoration of Fc receptor function. The chromatographic behavior and physical properties, its co-elution with anti-viral activity through a sequential purification scheme, the parallel activity of purified beta-interferon in enhancing both the binding and phagocytosis of EA, and the abrogation of factor-induced Fc-mediated phagocytosis with anti-Type II interferon antiserum, strongly support the hypothesis that the active factor is gamma- (Type II or immune) interferon (IFN). These studies suggest gamma-IFN may act as a differentiative signal to the macrophage by facilitating enhanced expression of macrophage surface membrane components.