Abstract
Food hypersensitivity is a group of diseases arising from a specific immune response that reproduces on exposure to a given food. The current understanding of molecular mechanisms and immunopathology of non-IgE-mediated/mixed food hypersensitivity, e.g., eosinophilic esophagitis, contains many gaps in knowledge. This review aims to provide a modern classification and identify the primary diseases of non-IgE-mediated/mixed food hypersensitivity reactions, delineate the distinctive molecular features, and discuss recent findings in the immunopathology of eosinophilic esophagitis that may become a basis to develop valid biomarkers and novel therapies for this disease. Eosinophilic esophagitis is a recently recognized allergic-mediated disease with eosinophil-predominant esophagus inflammation. Its pathogenesis is a complicated network of interactions and signaling between epithelial, mesenchymal, and immune cells on molecular and intercellular levels. Alterations produced by overactivation of some cytokine signaling pathways, e.g., IL-13 or thymic stromal lymphopoietin (TSLP), were evolved and observed in this review from the viewpoints of molecular, genetic, epigenetic, and transcriptomic changes. Despite substantial experimental data, the reliable and representative mechanism of eosinophilic esophagitis pathogenesis has yet to show itself. So, the place of esophagitis between mixed and non-IgE-mediated allergic disorders and between eosinophilic gastrointestinal disorders currently seems vague and unclear.
Highlights
Food hypersensitivity (FH) is a group of diseases arising from a specific immune response that reproduces on exposure to a given food
It can be hypothesized that the cadherin 26 (CDH26) increase in active Eosinophilic Esophagitis (EoE) and eosinophilic gastritis (EG) is involved in both promoting diseases, i.e., by increasing migration of some cell types that occur in inflamed mucosa and epithelium in EoE or by some other ways, and resolution of inflammation, inhibiting and dampening Th2–mediated activation to promote the return of the tissue to homeostasis
The reporter constructs assay revealed that the rs76562819 genetic variant was sufficient to produce genotype-dependent promoter activity highly similar to what is observed between risk and non–risk haplotypes in EoE patients, so it can be concluded that the rs76562819 EoE risk allele results in the decrease in IL13–induced CAPN14 expression in EoE patients
Summary
Food hypersensitivity (FH) is a group of diseases arising from a specific immune response that reproduces on exposure to a given food. IgE-mediated, non-IgE-mediated, and mixed food allergic (FA) reactions [1]. FH includes food pseudo-allergies (FPA), which are reactions that mimic FA, leading to the release of mediators, e.g., histamine but lack immunological mechanisms. The current understanding of non-IgE-mediated and mixed allergies (e.g., eosinophilic esophagitis (EoE)) molecular mechanisms and immunopathology contains many gaps in knowledge. Mediators in mast cell and basophil granules (histamine, serotonin, serine proteases and others), when released, cause vasodilatation, smooth muscle constriction, increase vascular permeability, producing FA symptoms, e.g., urticaria, angioedema, diarrhea and vomiting, bronchospasm, hypotension [6]. In mixed FA, both antigen-specific IgE and immune cells are involved in the reaction. Indirect-induced FPA is caused by foods containing histamine-releasing agents–COX inhibitors or histamine liberators. The pathogenesis of the action of histamine liberators is even less clear
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