ArticleThe Journal of investigative dermatology2015
The Tumor Necrosis Factor Superfamily Molecule LIGHT Promotes Keratinocyte Activity and Skin Fibrosis.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 53 citations in OpenAlex.
- Plasma Metabolomic and Proteomic Profiling of the Mechanisms Underlying the Cumulative Impact of Co-occurring Psychiatric Disorders on Atopic Dermatitis.Acta dermato-venereologica · 2026Article
- Tumor Necrosis Factor Superfamily 14: A Potential Predictor of Atrial Fibrillation Recurrence After Catheter Ablation.Clinical cardiology · 2026Article
- 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
- 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
- TNF superfamily control of tissue remodeling and fibrosis.Frontiers in immunology · 2023Review
- T cell co-stimulatory and co-inhibitory pathways in atopic dermatitis.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
- Realigning the LIGHT signaling network to control dysregulated inflammation.The Journal of experimental medicine · 2022Article
- Decoy receptor 3 is involved in epidermal keratinocyte commitment to terminal differentiation via EGFR and PKC activation.Experimental & molecular medicine · 2022Article
- LIGHT controls distinct homeostatic and inflammatory gene expression profiles in esophageal fibroblasts via differential HVEM and LTβR-mediated mechanisms.Mucosal immunology · 2022Article
- Inflammation and Interferon Signatures in Peripheral B-Lymphocytes and Sera of Individuals With Fibromyalgia.Frontiers in immunology · 2022Article
- Distal Lung Microenvironment Triggers Release of Mediators Recognized as Potential Systemic Biomarkers for Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2021Article
- Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14).Biomedicines · 2021Article
- Multimodal analysis for humaniScience · 2021Article
- Metabolic activation and colitis pathogenesis is prevented by lymphotoxin β receptor expression in neutrophils.Mucosal immunology · 2021Article
- Splenectomy improves liver fibrosis via tumor necrosis factor superfamily 14 (LIGHT) through the JNK/TGF-β1 signaling pathway.Experimental & molecular medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Several inflammatory diseases including scleroderma and atopic dermatitis display dermal thickening, epidermal hypertrophy, or excessive accumulation of collagen. Factors that might promote these features are of interest for clinical therapy. We previously reported that LIGHT, a TNF superfamily molecule, mediated collagen deposition in the lungs in response to allergen. We therefore tested whether LIGHT might similarly promote collagen accumulation and features of skin fibrosis. Strikingly, injection of recombinant soluble LIGHT into naive mice, either subcutaneously or systemically, promoted collagen deposition in the skin and dermal and epidermal thickening. This replicated the activity of bleomycin, an antibiotic that has been previously used in models of scleroderma in mice. Moreover skin fibrosis induced by bleomycin was dependent on endogenous LIGHT activity. The action of LIGHT in vivo was mediated via both of its receptors, HVEM and LTβR, and was dependent on the innate cytokine TSLP and TGF-β. Furthermore, we found that HVEM and LTβR were expressed on human epidermal keratinocytes and that LIGHT could directly promote TSLP expression in these cells. We reveal an unappreciated activity of LIGHT on keratinocytes and suggest that LIGHT may be an important mediator of skin inflammation and fibrosis in diseases such as scleroderma or atopic dermatitis.
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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.