• eosinophils;
  • IFN-γ receptor;
  • eosinophilic cationic protein;
  • CD69

In order to determine whether or not IFN-γR is associated with regulatory mechanisms on human eosinophil function, we examined the expression of functional IFN-γR on human peripheral eosinophils. In this study, peripheral blood eosinophils were obtained from seven normal controls and 12 patients (bronchial asthma, n = 9, and hypereosinophilic syndrome (HES), n = 3), and the purity of eosinophils was 97.11 ± 2. 31%, n = 19. We first showed that anti-IFN-γR α-chain MoAb reacted with all tested eosinophils of both normal controls and patients by flow cytometry analysis. We also showed expression of mRNA for the α-chain of IFN-γR in all purified eosinophils of six individuals. Further, to characterize IFN-γR on eosinophils, we did binding experiments with 125I-IFN-γ on purified peripheral eosinophils. The linear Scatchard plot indicated a single type of high-affinity binding sites (dissociation constant (Kd) = 3.89–4.95 × 10−10 M, numbers of binding sites = 183–233/cell, n = 3). To determine whether IFN-γR on eosinophils is functional, we examined surface eosinophilic cationic protein (ECP) and CD69 induction after IFN-γR ligation with recombinant human IFN-γ (rhIFN-γ) on eosinophils by flow cytometry. rhIFN-γ stimulation significantly induced both ECP and CD69 expression on the 2–18 h-cultured eosinophils in a dose-dependent manner. Further, the effects of rhIFN-γ stimulation were significantly blocked by both a neutralizing anti-IFN-γ MoAb and a blocking anti-IFN-γR MoAb. These results suggest that human peripheral eosinophils express functional IFN-γR.