Induction of Fc(ε) receptors on mouse macrophages and lymphocytes by homologous IgE

Normal mouse peritoneal macrophages express Fc(γ2a)R, Fc(γ1/2b)R, and Fc(ε)R, whereas B lymphocytes in mesenteric lymph nodes (MLN) bear Fc(γ2b)R, Fc(γ1), and Fc(ε)R. Rosette formation of Fc(ε)R⁺ macrophages and lymphocytes with IgE-coated ox erythrocytes was inhibited by rodent IgE but not by any other isotype of mouse immunoglobulins. In contrast, IgG1 rosettes and IgG2b rosettes of both macrophages and lymphocytes were inhibited not only by homologous isotype but also by IgE, suggesting that IgE has some affinity for Fc(γ1/2b)R on macrophages and for both Fc(γ1)R and Fc(γ2b)R on lymphocytes. Incubation of normal mouse macrophages with mouse IgE for 24 hr resulted in a twofold increase in the proportion of Fc(ε)R⁺ cells. Mouse IgE can induce Fc(ε)R on B cells as well. Incubation of MLN cells with mouse IgE for 2 to 4 hr, followed by culture of the cells in the absence of IgE, resulted in a 1.8- to 2.9-fold increase in Fc(ε)R⁺ cells. Determination of Fc(γ)R⁺ cells in the same MLN cells revealed that induction of Fc(ε)R by IgE was accompanied by a substantial decrease in the expression of Fc(γ1)R and Fc(γ2b)R. Induction of Fc(ε)R by IgE on macrophages and lymphocytes requires protein synthesis. In MLN cells, cycloheximide inhibited not only the IgE-induced increase in Fc(ε)R⁺ cells but also the decrease in Fc(γ1)R⁺ cells and Fc(γ2b)R⁺ cells. It was also found that induction of Fc(ε)R by IgE on macrophages was completely inhibited if IgG1 or IgG2b was added to the cells together with IgE. In contrast, IgG2a did not affect the IgE-induced expression of Fc(ε)R on macrophages. In MLN cells, IgG2b but not IgG1 inhibited both IgE-induced increase in Fc(ε)R and decrease in Fc(γ1)R and Fc(γ2b)R. The results indicate that expression of various Fc receptors on lymphocytes is mutually regulated.