BACKGROUND AND OBJECTIVE: Eosinophilic esophagitis (EoE) is an allergic disease of the esophagus. The IgE receptors on immune cells that infiltrate the esophagus are poorly defined. The high-affinity receptor for IgE, FcεRI, may play a role in EoE. The objective of the present study is to identify and compare the IgE receptors in the esophageal epithelium of patients with EoE, reflux esophagitis (RE), and normal controls. PATIENTS AND METHODS: A retrospective case-control study of 62 patients (19 EoE, 22 RE, 21 normal controls) was conducted. Biopsies were immunostained for FcεRI, CD23, galectin-3, c-kit, CD1a, and langerin. RESULTS: FcεRI was the only IgE receptor present in the esophageal epithelium of patients with EoE. The FcεRI-positive cell count varied by diagnosis (proximal biopsies EoE 32.6 ± 19.0 cells/high-power field, RE 26.7 ± 16.6, controls 15.6 ± 8.3, ANOVA P = 0.005; distal biopsies EoE 24.2 ± 16.2, RE 35.7 ± 27.6, controls 15.3 ± 8.4, P = 0.006). In the proximal esophagus, the FcεRI count was higher in EoE than in controls (P = 0.006); in the distal esophagus, the FcεRI count was higher in RE than in controls (P = 0.004). EoE and RE had similar FcεRI-positive cell counts. A subset of FcεRI-positive cells was similar in morphology and distribution to Langerhans cells (CD1a and langerin positive). CONCLUSIONS: The presence of FcεRI-positive cells in high numbers in the esophageal epithelium implies this receptor must be critical in the IgE-mediated activation of immune cells in the esophagus. Langerhans cells in the esophageal epithelium appear to express FcεRI. The role of Langerhans cells in the pathophysiology of EoE needs to be elucidated.
BACKGROUND AND OBJECTIVE:Eosinophilic esophagitis (EoE) is an allergic disease of the esophagus. The IgE receptors on immune cells that infiltrate the esophagus are poorly defined. The high-affinity receptor for IgE, FcεRI, may play a role in EoE. The objective of the present study is to identify and compare the IgE receptors in the esophageal epithelium of patients with EoE, reflux esophagitis (RE), and normal controls. PATIENTS AND METHODS: A retrospective case-control study of 62 patients (19 EoE, 22 RE, 21 normal controls) was conducted. Biopsies were immunostained for FcεRI, CD23, galectin-3, c-kit, CD1a, and langerin. RESULTS: FcεRI was the only IgE receptor present in the esophageal epithelium of patients with EoE. The FcεRI-positive cell count varied by diagnosis (proximal biopsies EoE 32.6 ± 19.0 cells/high-power field, RE 26.7 ± 16.6, controls 15.6 ± 8.3, ANOVA P = 0.005; distal biopsies EoE 24.2 ± 16.2, RE 35.7 ± 27.6, controls 15.3 ± 8.4, P = 0.006). In the proximal esophagus, the FcεRI count was higher in EoE than in controls (P = 0.006); in the distal esophagus, the FcεRI count was higher in RE than in controls (P = 0.004). EoE and RE had similar FcεRI-positive cell counts. A subset of FcεRI-positive cells was similar in morphology and distribution to Langerhans cells (CD1a and langerin positive). CONCLUSIONS: The presence of FcεRI-positive cells in high numbers in the esophageal epithelium implies this receptor must be critical in the IgE-mediated activation of immune cells in the esophagus. Langerhans cells in the esophageal epithelium appear to express FcεRI. The role of Langerhans cells in the pathophysiology of EoE needs to be elucidated.
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