ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2026
Oesophageal Epithelial Cell-Intrinsic MHCII Regulates Food Antigen-Dependent Eosinophilic Esophagitis in an IFNγ-Dependent Manner.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- The Immune Architecture of Eosinophilic Esophagitis: Mechanisms, Therapeutic Targets, and Precision Management.ImmunoTargets and therapy · 2026Review
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Abstract
backgroundEosinophilic oesophagitis (EoE) is a chronic food allergy that causes oesophageal inflammation and dysfunction. Recent work demonstrates IFNγ-dependent gene signatures in inflamed EoE biopsies. IFNγ has been implicated in the promotion of MHCII expression on oesophageal epithelial cells (EECs). However, the regulation of EEC-MHCII expression in vivo, and its contribution to EoE, is unknown.
objectiveThe objective of this study was to determine the regulation and role of EEC-intrinsic MHCII expression in EoE.
methodsWe examined the expression of HLA II-pathway transcripts in human EECs using single cell RNA-seq datasets and primary human tissues and mouse systems to interrogate the contribution of IFNγ to EEC-MHCII expression. Finally, we used a mouse disease model to test the contribution of epithelial MHCII to food antigen-dependent EoE.
resultsHLA II transcripts were upregulated in EECs of active EoE patients, compared with controls. Similarly, EEC-MHCII expression was higher in mice with EoE-like inflammation. EEC-MHCII expression was governed by IFNγ-responsive transcriptional regulation. EEC-specific MHCII deficiency resulted in exacerbated eosinophilic inflammation in a model of food antigen-dependent EoE.
conclusionWe find a novel immunoregulatory role for IFNγ-dependent EEC-MHCII in the context of oesophageal food allergy. CLINICAL RELEVANCE: Our results expand our understanding of oesophageal immune physiology and identify EEC-MHCII as mediating an anti-inflammatory axis that could be leveraged therapeutically.
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