ArticleThe Journal of allergy and clinical immunology2015
Tumor necrosis factor superfamily 14 (LIGHT) controls thymic stromal lymphopoietin to drive pulmonary fibrosis.
Article in The Journal of allergy and clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
- Parasite-Derived IL-33 Inhibitors Prevent Bleomycin-Induced Lung Fibrosis.European journal of immunology · 2026Article
- Tumor Necrosis Factor Superfamily 14: A Potential Predictor of Atrial Fibrillation Recurrence After Catheter Ablation.Clinical cardiology · 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
- TNFSF14-HVEM/LTβR Exacerbates Keratinocyte Abnormalities and IMQ-Induced Psoriatic Skin Inflammation via Activating NF-κB/TWIST1 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Combination therapy blocking TNF superfamily members 14 and 15 reverses pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Macrophages and Pulmonary Fibrosis.Current molecular medicine · 2025Review
- TSLP pretreatment inhibits M1 macrophage polarization and attenuates LPS-induced iNKT cell-dependent acute lung injury.Frontiers in immunology · 2025Article
- The Cellular and Transcriptomic Early Innate Immune Response to BCG Vaccination in Mice.Cells · 2024Article
- Article
- LIGHT signaling through LTβR and HVEM in keratinocytes promotes psoriasis and atopic dermatitis-like skin inflammation.Journal of autoimmunity · 2024Article
- 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
- A Deficiency in the Cytokine TNFSF14/LIGHT Limits Inflammation and Remodeling in Murine Eosinophilic Esophagitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- LIGHT deficiency attenuates acute kidney disease development in an in vivo experimental renal ischemia and reperfusion injury model.Cell death discovery · 2022Article
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms.Mucosal immunology · 2022Article
- Serum cytokine profiling reveals different immune response patterns during general and severeFrontiers in immunology · 2022Article
- Heterogeneity of ILC2s in the Intestine; Homeostasis and Pathology.Frontiers in immunology · 2022Review
- Conventional and pathogenic Th2 cells in inflammation, tissue repair, and fibrosis.Frontiers in immunology · 2022Review
- Distal Lung Microenvironment Triggers Release of Mediators Recognized as Potential Systemic Biomarkers for Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2021Article
- Large-scale plasma proteomics can reveal distinct endotypes in chronic obstructive pulmonary disease and severe asthma.Clinical and translational allergy · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPulmonary fibrosis is characterized by excessive accumulation of collagen and α-smooth muscle actin in the lung. The key molecules that promote these phenotypes are of clinical interest.
objectivesThymic stromal lymphopoietin (TSLP) has been found at high levels in patients with asthma and idiopathic pulmonary fibrosis, and TSLP has been proposed as a primary driver of lung fibrotic disease. We asked whether tumor necrosis factor superfamily protein 14 (TNFSF14) (aka LIGHT) controls TSLP production to initiate fibrosis.
methodsExpression of TSLP and initiation of pulmonary fibrosis induced by bleomycin were assessed in mice deficient in LIGHT. The ability of recombinant LIGHT, given intratracheally to naive mice, to promote TSLP and fibrosis was also determined.
resultsGenetic deletion of LIGHT abolished lung TSLP expression driven by bleomycin, accompanied by near-complete absence of accumulation of lung collagen and α-smooth muscle actin. Furthermore, recombinant LIGHT administered in vivo induced lung expression of TSLP in the absence of other inflammatory stimuli, and strikingly reproduced the primary features of bleomycin-driven disease in a TSLP-dependent manner. Blockade of LIGHT binding to either of its receptors, herpes virus entry mediator and lymphotoxin beta receptor, inhibited clinical symptoms of pulmonary fibrosis, and correspondingly both receptors were found on human bronchial epithelial cells, a primary source of TSLP. Moreover, LIGHT induced TSLP directly in human bronchial epithelial cells and synergized with IL-13 and TGF-β in vivo to promote TSLP in the lungs and drive fibrosis.
conclusionsThese results show that LIGHT is a profibrogenic cytokine that may be a key driver of TSLP production during the initiation and development of lung fibrotic disease.
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