ArticleNature medicine2011
The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
99 citing papers in PubMed, 171 citations in OpenAlex.
- Randomized, double-blind, controlled trial of human anti-LIGHT monoclonal antibody in COVID-19 acute respiratory distress syndrome.The Journal of clinical investigation · 2022Trial
- Tumor Necrosis Factor Superfamily 14: A Potential Predictor of Atrial Fibrillation Recurrence After Catheter Ablation.Clinical cardiology · 2026Article
- TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.The Journal of clinical investigation · 2026Article
- A Pilot Study on Early-Phase Efficacy and Biomarker Analysis of Cervical Intralymphatic Immunotherapy for Seasonal Rhinoconjunctivitis.Journal of asthma and allergy · 2026Article
- LIGHT in combination with IL-13 or IL-17 drives inflammatory transcriptional signatures in human pulmonary fibroblasts relevant for human lung disease.ImmunoHorizons · 2025Article
- Asthma Associated Cytokines Regulate Gasdermin A and Gasdermin B Expression by Human Bronchial Epithelial Cells.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- Combination therapy blocking TNF superfamily members 14 and 15 reverses pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Bidirectional Communication Between the Innate and Adaptive Immune Systems.Annual review of immunology · 2025Review
- BTLA agonist attenuates Th17-driven inflammation in a mouse model of steroid-resistant asthma.Frontiers in immunology · 2025Article
- Precision Medicine in Asthma: The Role of Biomarkers.ImmunoTargets and therapy · 2025Review
- Causal Relationship Between Immune Cells and Venous Thromboembolism: A Bidirectional Two-Sample Mendelian Randomization Study.Vascular health and risk management · 2025Article
- Muscular hyperplasia in Crohn's disease strictures: through thick and thin.American journal of physiology. Cell physiology · 2024Review
- PIP-seq identifies novel heterogeneous lung innate lymphocyte population activation after combustion product exposure.Scientific reports · 2024Article
- Cytotoxic CD4Med (New York, N.Y.) · 2023Article
- Exploring immune related gene signatures and mechanisms linking non alcoholic fatty liver disease to atrial fibrillation through transcriptome data analysis.Scientific reports · 2023Article
- A human model of asthma exacerbation reveals transcriptional programs and cell circuits specific to allergic asthma.Science immunology · 2023Article
- Lymphotoxin beta receptor signaling directly controls airway smooth muscle deregulation and asthmatic lung dysfunction.The Journal of allergy and clinical immunology · 2023Article
- TNF superfamily control of tissue remodeling and fibrosis.Frontiers in immunology · 2023Review
- LIGHT Amplification by NF-Mediators of inflammation · 2023Article
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Individuals with chronic asthma show a progressive decline in lung function that is thought to be due to structural remodeling of the airways characterized by subepithelial fibrosis and smooth muscle hyperplasia. Here we show that the tumor necrosis factor (TNF) family member LIGHT is expressed on lung inflammatory cells after allergen exposure. Pharmacological inhibition of LIGHT using a fusion protein between the IgG Fc domain and lymphotoxin β receptor (LTβR) reduces lung fibrosis, smooth muscle hyperplasia and airway hyperresponsiveness in mouse models of chronic asthma, despite having little effect on airway eosinophilia. LIGHT-deficient mice also show a similar impairment in fibrosis and smooth muscle accumulation. Blockade of LIGHT suppresses expression of lung transforming growth factor-β (TGF-β) and interleukin-13 (IL-13), cytokines implicated in remodeling in humans, whereas exogenous administration of LIGHT to the airways induces fibrosis and smooth muscle hyperplasia, Thus, LIGHT may be targeted to prevent asthma-related airway remodeling.
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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.