Abstract
BackgroundThe role of the high affinity IgE receptor, FcεRI, in IgE-mediated immune responses of the gastrointestinal (GI) mucosa is poorly understood. Currently, a detailed characterization of FcεRI expression throughout the human gut is lacking. The aim of this study was to define the expression pattern of FcεRI in the GI tract.Methods/Principal FindingsWe compared FcεRI expression in children with gastritis/esophagitis (n = 10), celiac disease (n = 10), inflammatory bowel disease (IBD) (n = 9), and normal mucosa (n = 5). The α–subunit of FcεRI (FcεRIα), detected by immunohistochemistry, was found on cells infiltrating the mucosa of the esophagus, the stomach, and the duodenum, but was rarely detected in more distal sections of the GI tract. Accordingly, quantitative RT-PCR analysis on esophagus, stomach, duodenum, colon, and rectum biopsies revealed that FcεRIα and -β expression levels decreased towards the distal intestine. mRNA transcripts of the common Fc-receptor-γ chain were present in the entire GI mucosa. Double-immunofluorescence staining of esophageal specimens confirmed that FcεRIα was expressed on intraepithelial mast cells and Langerhans cells. The mRNA expression levels of the α, β, and γ subunits of FcεRI did not correlate with total serum IgE but were associated with mucosal inflammation.Conclusion/SignificanceOur data define the upper GI tract as the main site for IgE-mediated immune activation via FcεRI. Tissue mRNA levels of FcεRIα are regulated by inflammatory conditions rather than serum IgE, indicating that FcεRI might also play a role in pathologies other than allergy.
Highlights
The gastrointestinal (GI) mucosa is a large interface area for pathogens and environmental antigens and, is under constant surveillance of the immune system
Patients had a diagnosis of gastritis/esophagitis (n = 10), celiac disease (n = 10), or inflammatory bowel disease (IBD) (n = 9)
We hypothesized that the mucosa of patients with inflammatory conditions of the gut should express high levels of FceRI transcripts due to the influx of inflammatory immune cells. In support of this hypothesis, we found that some gastritis/ esophagitis patients in our study showed higher FceRIa mRNA levels in the esophagus than celiac disease- and IBD-patients or normal controls (Figure 6A)
Summary
The gastrointestinal (GI) mucosa is a large interface area for pathogens and environmental antigens and, is under constant surveillance of the immune system. Humans express three IgE-receptors, the high affinity IgEreceptor, FceRI, and two low-affinity IgE receptors, FceRII (or CD23), and e-binding protein eBP (or galectin 3) [1]. In the human GI mucosa, the expression of the low affinity IgE receptors is well documented; CD23 is expressed on intestinal epithelial cells and functions as an antigen-sampling protein for IgE-antigen complexes, implying that CD23 plays a role in food allergy [2,3,4,5,6,7]. There is little data, on the expression profile of the high affinity receptor FceRI in the gastrointestinal mucosa. The role of the high affinity IgE receptor, FceRI, in IgE-mediated immune responses of the gastrointestinal (GI) mucosa is poorly understood. The aim of this study was to define the expression pattern of FceRI in the GI tract
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