ArticleGastroenterology2020
Increased Production of LIGHT by T Cells in Eosinophilic Esophagitis Promotes Differentiation of Esophageal Fibroblasts Toward an Inflammatory Phenotype.
Article in Gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Pooled it
- Dysregulated IL-2 signaling and T-cell subset shifts are associated with eosinophilic esophagitis activity.Biochemistry and biophysics reports · 2026Article
- Eosinophilic Esophagitis: Mechanisms of Disease and Approach to Treatment.Current allergy and asthma reports · 2026Review
- Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026Review
- Emerging Insights into the Inflammatory Phenotypes of Eosinophilic Esophagitis.Journal of inflammation research · 2026Review
- LIGHT in combination with IL-13 or IL-17 drives inflammatory transcriptional signatures in human pulmonary fibroblasts relevant for human lung disease.ImmunoHorizons · 2025Article
- The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025Review
- Eosinophilic esophagitis drives tissue fibroblast regenerative programs toward pathologic dysfunction.The Journal of allergy and clinical immunology · 2025Article
- Bidirectional Communication Between the Innate and Adaptive Immune Systems.Annual review of immunology · 2025Review
- Differential Contributions of Fibroblast Subpopulations to Intercellular Communication in Eosinophilic Esophagitis.Biology · 2024Article
- The TNFSF12/TWEAK Modulates Colonic Inflammatory Fibroblast Differentiation and Promotes Fibroblast-Monocyte Interactions.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024Review
- Association of TNFRSF19 with a TNF family-based prognostic model and subtypes in gliomas using machine learning.Heliyon · 2024Article
- LIGHT signaling through LTβR and HVEM in keratinocytes promotes psoriasis and atopic dermatitis-like skin inflammation.Journal of autoimmunity · 2024Article
- Eosinophilic esophagitis: Shifting immune complexity beyond the eosinophil.The Journal of allergy and clinical immunology · 2024Article
- The New Therapeutic Frontiers in the Treatment of Eosinophilic Esophagitis: Biological Drugs.International journal of molecular sciences · 2024Review
- Eosinophilic esophagitis in the "atopic march": dupilumab as an "umbrella" strategy for multiple coexisting atopic diseases.Frontiers in medicine · 2024Review
- Mechanistic Insights into Eosinophilic Esophagitis: Therapies Targeting Pathophysiological Mechanisms.Cells · 2023Review
- TNFSF14/LIGHT promotes cardiac fibrosis and atrial fibrillation vulnerability via PI3Kγ/SGK1 pathway-dependent M2 macrophage polarisation.Journal of translational medicine · 2023Article
- Lymphotoxin beta receptor signaling directly controls airway smooth muscle deregulation and asthmatic lung dysfunction.The Journal of allergy and clinical immunology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 8 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsEosinophilic esophagitis (EoE) is an antigen-mediated eosinophilic disease of the esophagus that involves fibroblast activation and progression to fibrostenosis. Cytokines produced by T-helper type 2 cells and transforming growth factor beta 1 (TGFβ1) contribute to the development of EoE, but other cytokines involved in pathogenesis are unknown. We investigate the effects of tumor necrosis factor superfamily member 14 (TNFSF14, also called LIGHT) on fibroblasts in EoE.
methodsWe analyzed publicly available esophageal CD3
resultsLIGHT was up-regulated in the esophageal tissues from patients with EoE, compared with control individuals, and expressed by several T-cell populations, including T-helper type 2 cells. TNF receptor superfamily member 14 (TNFRSF14, also called HVEM) and lymphotoxin beta receptor are receptors for LIGHT that were expressed by fibroblasts from healthy donors or patients with active EoE. Stimulation of esophageal fibroblasts with LIGHT induced inflammatory gene transcription, whereas stimulation with TGFβ1 induced transcription of genes associated with a myofibroblast phenotype. Stimulation of fibroblasts with TGFβ1 increased expression of HVEM; subsequent stimulation with LIGHT resulted in their differentiation into cells that express markers of myofibroblasts and inflammatory chemokines and cytokines. Eosinophils tethered to esophageal fibroblasts after LIGHT stimulation via intercellular adhesion molecule-1.
conclusionsT cells in esophageal tissues from patients with EoE express increased levels of LIGHT compared with control individuals, which induces differentiation of fibroblasts into cells with inflammatory characteristics. TGFβ1 increases fibroblast expression of HVEM, a receptor for LIGHT. LIGHT mediates interactions between esophageal fibroblasts and eosinophils via ICAM1. This pathway might be targeted for the treatment of EoE.
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What OpenQuestion holds
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.