1978Kitakantou igaku/Kitakantō IgakuOpen access

ACTIVATION OF CYTOTOXIC MACROPHAGE WITH MACROPHAGE

Saburo Yamamoto

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Abstract

Mouse peritoneal exudate macrophages induced by peptone (macrophages) were activated with a lymphokine, macrophage activating factor (MAF), and became cytotoxic against various tumor cells. Peritoneal resident adherent-cells from normal mice were not activated with MAF.When macrophages were incubated with aggregated human immunoglobulin G (agg-HGG) for 30 min, they showed no response to MAF. The preventing effect of agg-HGG depended on the doses of HGG added. Agg-BGG also prevented the macrophage activation with MAF. On the contrary, pretreatment of macrophages with heated BSA or monomeric HGG exibited no effect on macrophage activation with MAF. Pretreatment with the Fc rich fraction eliminated the responsiveness of macrophages to MAF, while pretreatment with F (ab')2 rich fraction did not. These facts suggest that the inhibition is caused by the interaction of Fc receptor with Fc portion of immunoglobulin G.Post-treatment of activated macrophages with HGG did not influence on the cytotoxic activity. MAF was adsorbed onto the macrophages, which had been pretreated with agg-HGG, as well as to the untreated macrophages. This fact indicate that the binding of HGG to Fc receptor does not interfere the interaction of MAF receptors and MAF molucules.Then, the author speculate possible inhibiting mechanism of IgG on the macrophage activation with MAF as follow : the binding of Fc portion may trigger a central off signal to macrophage activation with MAF.

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Mouse peritoneal exudate macrophages induced by peptone (macrophages) were activated with a lymphokine, macrophage activating factor (MAF), and became cytotoxic against various tumor cells. Peritoneal resident adherent-cells from normal mice were not activated with MAF.When macrophages were incubated with aggregated human immunoglobulin G (agg-HGG) for 30 min, they showed no response to MAF. The preventing effect of agg-HGG depended on the doses of HGG added. Agg-BGG also prevented the macrophage activation with MAF. On the contrary, pretreatment of macrophages with heated BSA or monomeric HGG exibited no effect on macrophage activation with MAF. Pretreatment with the Fc rich fraction eliminated the responsiveness of macrophages to MAF, while pretreatment with F (ab')2 rich fraction did not. These facts suggest that the inhibition is caused by the interaction of Fc receptor with Fc portion of immunoglobulin G.Post-treatment of activated macrophages with HGG did not influence on the cytotoxic activity. MAF was adsorbed onto the macrophages, which had been pretreated with agg-HGG, as well as to the untreated macrophages. This fact indicate that the binding of HGG to Fc receptor does not interfere the interaction of MAF receptors and MAF molucules.Then, the author speculate possible inhibiting mechanism of IgG on the macrophage activation with MAF as follow : the binding of Fc portion may trigger a central off signal to macrophage activation with MAF.

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Available abstract

Mouse peritoneal exudate macrophages induced by peptone (macrophages) were activated with a lymphokine, macrophage activating factor (MAF), and became cytotoxic against various tumor cells. Peritoneal resident adherent-cells from normal mice were not activated with MAF.When macrophages were incubated with aggregated human immunoglobulin G (agg-HGG) for 30 min, they showed no response to MAF. The preventing effect of agg-HGG depended on the doses of HGG added. Agg-BGG also prevented the macrophage activation with MAF. On the contrary, pretreatment of macrophages with heated BSA or monomeric HGG exibited no effect on macrophage activation with MAF. Pretreatment with the Fc rich fraction eliminated the responsiveness of macrophages to MAF, while pretreatment with F (ab')2 rich fraction did not. These facts suggest that the inhibition is caused by the interaction of Fc receptor with Fc portion of immunoglobulin G.Post-treatment of activated macrophages with HGG did not influence on the cytotoxic activity. MAF was adsorbed onto the macrophages, which had been pretreated with agg-HGG, as well as to the untreated macrophages. This fact indicate that the binding of HGG to Fc receptor does not interfere the interaction of MAF receptors and MAF molucules.Then, the author speculate possible inhibiting mechanism of IgG on the macrophage activation with MAF as follow : the binding of Fc portion may trigger a central off signal to macrophage activation with MAF.

Key concepts: Macrophage, Macrophage-activating factor, Cytotoxic T cell, Lymphokine, Fc receptor, Receptor, Chemistry, Antibody

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