Low-affinity receptor for IgE on human bronchial epithelial cells in asthma.

AM Campbell, AM Vignola, P Chanez, P Godard… - …, 1994 - ncbi.nlm.nih.gov
AM Campbell, AM Vignola, P Chanez, P Godard, J Bousquet
Immunology, 1994ncbi.nlm.nih.gov
Bronchial epithelial cells are activated in asthma but the mechanisms underlying this
activation are poorly understood. We tested the possibility that bronchial epithelial cells
recovered by brushing from 15 asthmatic and 11 control subjects may be activated by an IgE-
dependent mechanism. The expression of the low-affinity IgE receptor (CD23) was studied
by immunocytochemistry using the alkaline phosphatase anti-alkaline phosphatase
technique and immunofluorescence using confocal microscopy. Four of eight allergic …
Abstract
Bronchial epithelial cells are activated in asthma but the mechanisms underlying this activation are poorly understood. We tested the possibility that bronchial epithelial cells recovered by brushing from 15 asthmatic and 11 control subjects may be activated by an IgE-dependent mechanism. The expression of the low-affinity IgE receptor (CD23) was studied by immunocytochemistry using the alkaline phosphatase anti-alkaline phosphatase technique and immunofluorescence using confocal microscopy. Four of eight allergic asthmatic patients and none of the seven non-allergic asthmatic or control subjects had a positive expression of CD23. The functional activity of CD23 was examined in the cells recovered from these subjects by stimulating them with IgE/anti-IgE. 15-HETE was not released but endothelin was released in the three or four asthmatic patients who had a positive expression of CD23. None of the other subjects released any endothelin. This study suggests that bronchial epithelial cells of asthmatic patients may be directly activated by an IgE-mediated mechanism.
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