Regulation of cell surface FcεRI expression by IgE. Implication in allergy

We investigated whether IL-4 and IgE regulate surface expression and function of FcεRI ineosinophils,Eosinophils were purified from venous blood from consenting volunteers with no . Eosinophils were from venous blood from consenting volunteers with nohistory of atopic diseases. Cells were cultured with IL-5and with or without IL-4 and/or IgE at 37℃. After culture for 7 days，the surface FcεRI expression on eosinophils was分析by flow cytometry using anti-FcεRI mAb，crab -1. Although peripheral blood eosinophils did not express surface FcεRI，apparent FcεRI expression (up to 1% of mast cell FcεRI levels) was observed in eosinophils cultured与both IL-4和IgE from all donors. The combination of IL-4和IgB was necessary for Themaximal induction of surface FcεRI expression. In the presence of IL-4 and IgE，eosinophils cultured for 2 days demonstrated low but statistically significant levels of surfaceFcεRI，其中reached to plateau after 7 days of culture. However，cross-linking of surface FcεRI by cra1 failed to induce the release of eosiaophil-derivedneurotoxin (EDN) or leukotriene (LT) C4，or Ca D12+ D1 influx in eosinophils cultured for 7 days with IL-4 and IgE. These results suggestthat surface FcεRI expression in eosinophils is regulated by a mechanism similar to that in mastcells。

We investigated whether IL-4 and IgE regulate surface expression and function of FcεRI in eosinophils, as with mast cells. Eosinophils were purified from venous blood from consenting volunteers with no history of atopic diseases. Cells were cultured with IL-5, and with or without IL-4 and/or IgE at 37℃. After culture for 7 days, the surface FcεRI expression on eosinophils was analyzed by flow cytometry using anti-FcεRI mAb, CRA-1. Although peripheral blood eosinophils did not express surface FcεRI, apparent FcεRI expression (up to 1% of mast cell FcεRI levels) was observed in eosinophils cultured with both IL-4 and IgE from all donors. The combination of IL-4 and IgB was necessary for the maximal induction of surface FcεRI expression. In the presence of IL-4 and IgE, eosinophils cultured for 2 days demonstrated low but statistically significant levels of surface FcεRI, which reached to plateau after 7 days of culture. However, cross-linking of surface FcεRI by CRA-1 failed to induce the release of eosiaophil-derived neurotoxin (EDN) or leukotriene (LT) C4, or CaィイD12+ィエD1 influx in eosinophils cultured for 7 days with IL-4 and IgE. These results suggest that surface FcεRI expression in eosinophils is regulated by a mechanism similar to that in mast cells.