Fc receptors (FcR) are of importance in immune and inflammatory reactions. FcR expression as mRNA and surface protein was therefore examined in the myelomonocytic cell line, U937, after stimulation with phorbol ester (PMA), in the presence of seven different cytokines (interferon‐γ [IFNγ], IFNα, granulocyte‐macrophage colony‐stimulating factor [GM–CSF], tumour necrosis factor‐α [TNFα], TNFβ, interleukin‐β [IL‐1β], IL‐2) or dexamethasone. HLA class I and CD lib expression were also examined. Cell surface expression of FcRI and II was measured by flow cytometry using monoclonal antibodies, and the mRNA of FcRII was measured with cDNA or oligonucleotide probes. The major findings were: PMA increased cell surface FcRI, FcRII and CD11b, but decreased HLA; PMA caused a fivefold increase in all three FcRII RNA transcripts (2.5, 1.5 and 0.9 kb) in Northern analysis; IFNγ, IFNα and GM‐CSF increased the expression of FcRI and II, and there was no effect with IL‐1β, IL‐2, TNFα or TNFβ (only GM‐CSF increased the expression of CD11b); all cytokines further increased FcRI and FcRII expression in the presence of PMA; HLA expression was also increased in the presence of PMA, IFNα and IFNγ; dexamethasone reduced the levels of FcRI and II in cells stimulated with PMA with or without cytokines. Thus stimulatory agents and cytokines can alter the expression of surface FcγR and mRNA encoding FcRI or II, providing potential control mechanisms for the modulation of these receptors in inflammatory responses.