Expression of the high-affinity IgE receptor on peripheral blood dendriticcells: Differential binding of IgE in atopic asthma

Citation
Ja. Holloway et al., Expression of the high-affinity IgE receptor on peripheral blood dendriticcells: Differential binding of IgE in atopic asthma, J ALLERG CL, 107(6), 2001, pp. 1009-1018
Citations number
26
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
107
Issue
6
Year of publication
2001
Pages
1009 - 1018
Database
ISI
SICI code
0091-6749(200106)107:6<1009:EOTHIR>2.0.ZU;2-V
Abstract
Background: Dendritic cells can express the high-affinity IgE receptor (Fc epsilon RI), which, in the presence of specific IgE, facilitates the uptake of allergen, leading to increased activation of allergen-specific T tells. FceRI expression by dendritic cells is higher in the airways of atopic ast hmatic subjects than in those of healthy, nonatopic control subjects. Objective: The aims of this study were to determine whether a similar diffe rence in Fc epsilon RI expression occurs between dendritic cells in the per ipheral blood of atopic asthmatic subjects and healthy individuals and also whether an altered ability of Fc epsilon RI+ peripheral blood dendritic ce lls to bind IgE accompanies the atopic asthmatic state. Methods: Flow cytometry was used to analyze the surface expression of Fc ep silon RI and exogenously bound IgE on dendritic tells identified as lineage negative (CD3, CD14, CD16, CD19, and CD56) and HLA-DR bright. Results: The total expression of Fc epsilon RI 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 Fc epsilon RI on peripheral blood dendritic cells from healthy and asthmatic subjects suggest that the local environment in the airway is responsible for the upregulation of sur face FceRI on airway dendritic cells in asthma, The results also suggest th at the functional ability of FceRI to bind IgE is differentially controlled in the atopic state.