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Correction of defective macrophage differentiation in C3H/HeJ mice by an interferon-like molecule
Abstract:
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.
Insights
Cultured macrophages from C3H/HeJ mice regain Fc receptor function after treatment with a specific lymphokine. This factor, identified as gamma-interferon (IFN), restores the ability of macrophages to bind and phagocytose opsonized sheep erythrocytes.
Area of Science:
- Immunology
- Cell Biology
Background:
- C3H/HeJ mouse macrophages lose Fc receptor function in culture.
- This defect impairs their ability to bind and phagocytose opsonized targets.
Purpose of the Study:
- To identify the factor in Con A-stimulated spleen cell supernatant that restores Fc receptor function.
- To biochemically and functionally characterize this active factor.
Main Methods:
- Biochemical analysis including chromatography.
- Functional assays measuring erythrocyte binding and phagocytosis.
- Interferon characterization and neutralization studies.
Main Results:
- A lymphokine-rich supernatant restored Fc receptor function in cultured macrophages.
- The active factor co-eluted with antiviral activity and purified beta-interferon.
- Anti-Type II interferon antiserum abrogated the restorative effect.
Conclusions:
- The active factor is identified as gamma-interferon (Type II interferon).
- Gamma-interferon likely acts as a differentiative signal, enhancing macrophage Fc receptor expression and function.