ArticleJCI insight2023
Suprabasal cells retain progenitor cell identity programs in eosinophilic esophagitis-driven basal cell hyperplasia.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Cellular and molecular dysregulation of the esophageal epithelium in systemic sclerosis.JCI insight · 2026Article
- ProtoCloud: A prototypical self-explaining model for single-cell analysis.Cell genomics · 2026Article
- Article
- Eosinophilic Esophagitis: Mechanisms of Disease and Approach to Treatment.Current allergy and asthma reports · 2026Review
- Proton pump inhibitors modulate esophageal epithelial barrier function and crosstalk with eosinophils.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- Oesophageal Epithelial Cell-Intrinsic MHCII Regulates Food Antigen-Dependent Eosinophilic Esophagitis in an IFNγ-Dependent Manner.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- Epithelial pyroptosis-induced TREM1Cell death discovery · 2025Article
- FOXM1 Modulation Alleviates Epithelial Remodeling and Inflammation in Eosinophilic Esophagitis.bioRxiv : the preprint server for biology · 2025Article
- Esophageal epithelial Ikkβ deletion promotes eosinophilic esophagitis in experimental allergy mouse model.The Journal of allergy and clinical immunology · 2025Article
- An AI-assisted morphoproteomic approach is a supportive tool in esophagitis-related precision medicine.EMBO molecular medicine · 2025Article
- Advances in omics data for eosinophilic esophagitis: moving towards multi-omics analyses.Journal of gastroenterology · 2024Review
- Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Eosinophilic esophagitis (EoE) is an esophageal immune-mediated disease characterized by eosinophilic inflammation and epithelial remodeling, including basal cell hyperplasia (BCH). Although BCH is known to correlate with disease severity and with persistent symptoms in patients in histological remission, the molecular processes driving BCH remain poorly defined. Here, we demonstrate that BCH is predominantly characterized by an expansion of nonproliferative suprabasal cells that are still committed to early differentiation. Furthermore, we discovered that suprabasal and superficial esophageal epithelial cells retain progenitor identity programs in EoE, evidenced by increased quiescent cell identity scoring and the enrichment of signaling pathways regulating stem cell pluripotency. Enrichment and trajectory analyses identified SOX2 and KLF5 as potential drivers of the increased quiescent identity and epithelial remodeling observed in EoE. Notably, these alterations were not observed in gastroesophageal reflux disease. These findings provide additional insights into the differentiation process in EoE and highlight the distinct characteristics of suprabasal and superficial esophageal epithelial cells in the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.