Human HMC-1 mast cells exclusively express the FcγRII subtype of IgG receptor

Abstract

Because of their localization at the interface of the internal and external environment mast cells play a crucial role in the immune response and in inflammatory reactions. Effects may be mediated not only by the high-affinity IgE receptor, but also by IgG receptors. Since in rodent mast cells signal transduction via the Fcγ receptor family has been shown, we analysed the expression of surface receptors for IgG on the human mast cell line HMC-1. It was shown by flow cytometric analysis that HMC-1 constitutively expressed the FcγRII/CD32 subtype whereas FcγRI/CD64 and FcγRIII/CD16 were not expressed. This exclusive expression of the FcγRII subtype of IgG receptor is similar to the expression pattern of basophils, although concerning cell surface molecules HMC-1 rather seem to resemble monocytes. In contrast to monocytes the expression profile on HMC-1 did not change upon stimulation with IL-4, TNFα, IFNγ, PMA or salbutamol. Moreover, the mast cell-activating cytokine SCF and the calcium ionophore A23187 did not modulate the FcγR profile in this study. To assess the importance of the exclusive FcγRII expression on HMC-1, we investigated whether the production of the cytokine TNFα is modulated via FcγRII activation or if an increase in intracellular calcium could be observed. No significant modulation of TNFα release or of intracellular free calcium after crosslinking of FcγRII by heat-aggregated IgG or by a second antibody was observed. It remains to be clarified whether this low-affinity subtype for the IgG receptor is involved in antigen-dependent sensitization of human tissue mast cells resulting in secretion of immunoregulatory cytokines. This mechanism may be important for disease states associated with circulating or tissue-bound immune complexes.