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
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
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.