Intestinal IgE secretion in food allergy: Potential role for CD23 isoforms on intestinal epithelial cells

Abstract

Rationale Anaphylactic reactions can occur extremely rapidly after ingestion of food allergens. A CD23/IgE-dependent antigen uptake mechanism is required for rapid hypersensitivity reactions in rodent models of food allergy. The mechanism leading to lumenal IgE remains unknown. Methods Naïve and sensitized (OVA and casein) C3H/HeJ mice were used. Specific IgE was measured in intestinal lavage from mice, and in stool samples from food allergic patients. Intestinal secretion of IgE and IgG were compared by injection of mice with 125I-IgE or -IgG and measurement of 125I in intestinal lavage and stool. CD23 expression was determined by immunohistochemistry and RT-PCR. IgE uptake by intestinal epithelial cells (IEC) was determined by confocal microscopy. Results Allergen-specific IgE was detected in stool samples from food-allergic patients, and in intestinal lavage fluid from sensitized mice. Sensitized mice secreted greater levels of 125I-IgE, and to a lesser extent 125I-IgG, into the intestinal lumen compared to naïve mice. Sensitization was associated with upregulated CD23 expression on mouse IEC. RT-PCR analysis of CD23 isoform expression in IEC obtained from patients with food allergic disorders or normal controls demonstrated that the CD23a isoform was constitutively expressed, while the CD23b isoform was present only in IEC from food allergic patients. Polarized caco-2 cells transfected with the CD23a isoform rapidly internalized FITC-IgE from the apical, but not the basolateral domain. Conclusions Allergen-specific IgE is secreted into the intestinal lumen in sensitized individuals, and may facilitate uptake of antigen by interaction with CD23a. Upregulation of the CD23b isoform may be responsible for the secretion of IgE into the intestinal lumen.