Expression of the high-affinity IgE receptor on peripheral blood dendritic cells: differential binding of IgE in atopic asthma

Holloway, Judith A., Holgate, Stephen T. and Semper, Amanda E. (2001) Expression of the high-affinity IgE receptor on peripheral blood dendritic cells: differential binding of IgE in atopic asthma. Journal of Allergy and Clinical Immunology, 107 (6), 1009-1018. (doi:10.1067/mai.2001.115039).

Abstract

Background: Dendritic cells can express the high-affinity IgE receptor (FcεRI), which, in the presence of specific IgE, facilitates the uptake of allergen, leading to increased activation of allergen-specific T cells. FcεRI expression by dendritic cells is higher in the airways of atopic asthmatic subjects than in those of healthy, nonatopic control subjects.
Objective: The aims of this study were to determine whether a similar difference in FcεRI expression occurs between dendritic cells in the peripheral blood of atopic asthmatic subjects and healthy individuals and also whether an altered ability of FcεRI⁺ peripheral blood dendritic cells to bind IgE accompanies the atopic asthmatic state.
Methods: Flow cytometry was used to analyze the surface expression of FcεRI and exogenously bound IgE on dendritic cells identified as lineage negative (CD3, CD14, CD16, CD19, and CD56) and HLA-DR bright.
Results: The total expression of FcεRI on the surface of dendritic cells from healthy and asthmatic subjects was not significantly different. However, in vivo, dendritic cells from atopic asthmatic subjects had higher levels of receptor occupancy by IgE and bound exogenous IgE in vitro more efficiently than dendritic cells from healthy subjects.
Conclusion: The similar levels of expression of FcεRI on peripheral blood dendritic cells from healthy and asthmatic subjects suggest that the local environment in the airway is responsible for the upregulation of surface FcεRI on airway dendritic cells in asthma. The results also suggest that the functional ability of FcεRI to bind IgE is differentially controlled in the atopic state.

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Contributors

Author: Judith A. Holloway

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