ENHANCED EXPRESSION OF HIGH-AFFINITY IGE RECEPTOR (FC-EPSILON-RI) A CHAIN IN HUMAN ALLERGEN-INDUCED RHINITIS WITH COLOCALIZATION TO MAST-CELLS, MACROPHAGES, EOSINOPHILS, AND DENDRITIC CELLS

Citation
K. Rajakulasingam et al., ENHANCED EXPRESSION OF HIGH-AFFINITY IGE RECEPTOR (FC-EPSILON-RI) A CHAIN IN HUMAN ALLERGEN-INDUCED RHINITIS WITH COLOCALIZATION TO MAST-CELLS, MACROPHAGES, EOSINOPHILS, AND DENDRITIC CELLS, Journal of allergy and clinical immunology, 100(1), 1997, pp. 78-86
Citations number
32
Categorie Soggetti
Immunology,Allergy
ISSN journal
00916749
Volume
100
Issue
1
Year of publication
1997
Pages
78 - 86
Database
ISI
SICI code
0091-6749(1997)100:1<78:EEOHIR>2.0.ZU;2-D
Abstract
Background: IgE-dependent activation of mast cells and basophils throu gh the high-affinity IgE receptor (Fc epsilon RI) is involved in the p athogenesis of allergen-induced immediate and late responses. Objectiv e: We investigated the expression and cellular distribution of Fc epsi lon RI in the nasal mucosa after allergen challenge in patients with s ummer hay fever. Methods: Fourteen grass pollen-sensitive patients and seven normal control subjects underwent nasal challenge with grass po llen and allergen diluent in random order separated by 2 weeks. Nasal airway caliber was monitored by acoustic rhinometry, and nasal biopsy was performed at 6 hours. Messenger RNA for Fc epsilon RI was determin ed by using reverse-transcription polymerase chain reaction, and Fc ep silon RI protein-expression was determined by immunohistology with a m ouse monoclonal antibody (22E7) and a rabbit polyclonal antibody (997) directed against the or subunit. Co-localization of Fc epsilon RI rec eptors was performed by using double-immunostaining methods. Results: In atopic subjects, there was a significant early decrease in nasal ai rway caliber, which extended up to 6 hours after allergen challenge. F c epsilon RI mRNA levels were elevated at 6 hours (p = 0.03). Cells ex pressing Fc epsilon RI protein were increased in patients with atopic rhinitis compared with normal control subjects (p = 0.03). Further inc reases in Fc epsilon RI+ cells were observed after allergen challenge only in the atopic group (p = 0.02). Double immunohistochemistry revea led that the majority of Fc epsilon RI+ cells were mast cells (64%), f ollowed by macrophages (20%), eosinophils (4%), and dendritic cells (2 %), with 10% Fc epsilon RI+ cells being unidentified. Conclusions: Our results demonstrate increased Fc epsilon RI expression during allerge n induced rhinitis and highlight a potential target for treatment.