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We investigated the effects of interferon-gamma (IFN-gamma), phorbol myristate acetate (PMA), and dibutyryl cAMP (Bt2cAMP) on Fc gamma R subtype expression on a human eosinophilic leukemia cell line, EoL-3. Unstimulated EoL-3 cells expressed Fc gamma RII as determined by monoclonal antibody (mAb) IV-3, whereas there was little or no Fc gamma RI and Fc gamma RIII expression as determined by mAbs 32.2 and 3G8, respectively. IFN-gamma induced Fc gamma RI expression, and Bt2 cAMP, which did not induce Fc gamma RI expression by itself, showed an additive effect on IFN-gamma-induced Fc gamma RI expression. Fc gamma RII expression was augmented by IFN-gamma, PMA, and Bt2 cAMP. Bt2 cAMP also showed an additive effect on IFN-gamma-augmented Fc gamma RII expression. Fc gamma RIII expression could be induced only by IFN-gamma plus Bt2 cAMP. H-7, a protein kinase C (PK-C) inhibitor, suppressed the enhancement of Fc gamma R subtype expression induced by these reagents. These results show that Fc gamma R subtype expression on EoL-3 cells is regulated differently in each subtype and that cAMP and PK-C play important roles in the regulation.

Regulation of low-affinity receptors for IgE (Fc epsilon R2/CD23) on a human eosinophilic cell line EoL3 and a human monocytic cell line U937 was studied using an anti-Fc,R2/CD23 monoclonal antibody H107 by flow cytometry. While platelet-activating factor, interleukin 4, and interferon gamma significantly augmented Fc epsilon R2/CD23 expression on both cell lines, transforming growth factor beta (TGF beta) inhibited both the basal level of Fc epsilon R2/CD23 expression and the enhanced Fc epsilon R2/CD23 expression induced by these reagents in dose- and time-dependent manners. However, TGF beta did not significantly suppress the high basal level of Fc epsilon R2/CD23 expression on RPMI 8866 cells. These results suggest that Fc epsilon R2/CD23 expression on EoL3 and U937 cells is regulated by various cytokines and growth factors, and that TGF beta plays an important regulatory role in IgE-mediated immune responses.