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Expression of the high affinity IgE receptor (Fc epsilon RI) on eosinophils has recently been reported. This led us to evaluate Fc epsilon RI expression on eosinophils in atopic dermatitis (AD). Double immunofluorescence stainings with an anti-Fc epsilon RI monoclonal antibody (mAb) and a polyclonal antieosinophil cationic protein (ECP) antibody were performed on lesional biopsy specimens from patients with AD and from patients with bullous pemphigoid (BP) as controls. In AD and BP lesions, 77% and 70% of eosinophils expressed Fc epsilon RI, respectively. However, the intensity of Fc epsilon RI staining in AD was much stronger than in BP, suggesting upregulation of Fc epsilon RI expression on eosinophils in AD. In addition, the eosinophils infiltrating AD lesions were stained strongly with anti-CD23 mAb and anti-IgE antibody. At the sites of mite patch testing in AD, Fc epsilon RI-, CD23- and IgE-positive eosinophils were observed to the same degree as in the lesions, and a considerable number of mite antigen-bearing eosinophils were detected. Fc epsilon RI and CD23 were both upregulated on the skin-infiltrating eosinophils in AD and bound IgE molecules.

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High affinity IgE receptor (Fc ε R I) expression on monocytes and its upregulation on monocytes from patients with atopic dermatitis (AD) have been recently reported. In this study, we investigated whether prostaglandin E2 (PGE2) release from AD monocytes was Fc ε R I-dependent or not. The monocytes were stimulated with anti-Fc ε RI monoclonal antibody (mAb) and anti-Fc ε RII mAb. Cross-linking of Fc ε R I, but not that of Fc ε R II induced PGE2 release from monocytes. In order to confirm that the PGE2 release is IgE-dependent, stimulation with IgE+anti-IgE, IgG+anti-IgG and immune complexes made by incubation with AD patients’ serum and recombinant Der f ll (rDer f ll-lC) were carried out in the culture. Significant PGE2 release by all the stimulants was observed, as compared with spontaneous release. PGE2 release by immune complex made by incubation with IgE-absorbed AD serum and rDer f ll was much lower than that by rDer f Il-lC. In monocytes from nonatopic donors, significant PGE2 release was observed when stimulated with IgE+anti-IgE, IgG+anti-IgG, rDer f II-lC, but not with anti-FC ε RI mAb and anti-Fc ε RII mAb. However, the release were significantly lower than respective PGE2 releases from AD monocytes. Taken together, cross-linking of Fc ε R I and IgE induced a PGE2 release from monocytes. This is a first report demonstrating an Fc ε R I-dependent mediator release from monocytes of AD patients.