ArticleThe Journal of clinical investigation2006
Essential role of TNF family molecule LIGHT as a cytokine in the pathogenesis of hepatitis.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Lymphotoxin-beta receptor controls the development of chronic pain.Cell reports · 2026Article
- NTX250: A Modular mRNA-Based Immunotherapy Platform for HPV-Associated Cancers with Broad Applicability.bioRxiv : the preprint server for biology · 2025Article
- Intrathecal Inflammatory Profile and Gray Matter Damage Predict Progression Independent of Relapse Activity in Early Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Revealing the mechanisms and therapeutic potential of immune checkpoint proteins across diverse protein families.Frontiers in immunology · 2025Review
- Kupffer Cells and Hepatocytes: A Key Relation in the Context of Canine Leishmaniasis.Microorganisms · 2024Article
- Review
- LIGHT Amplification by NF-Mediators of inflammation · 2023Article
- Unravelling the unsolved paradoxes of cytokine families in host resistance and susceptibility toCytokine: X · 2020Article
- Article
- Increased LIGHT leading to sFlt-1 elevation underlies the pathogenic link between hydatidiform mole and preeclampsia.Scientific reports · 2019Article
- Pathological significance and regulatory mechanism of lymphotoxin β receptor overexpression in T cells of patients with systemic lupus erythematosus.Journal of biomedical research · 2018Article
- LIGHT-HVEM signaling in keratinocytes controls development of dermatitis.The Journal of experimental medicine · 2018Article
- A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice.Nature communications · 2016Article
- LIGHT/TNFSF14 is increased in patients with type 2 diabetes mellitus and promotes islet cell dysfunction and endothelial cell inflammation in vitro.Diabetologia · 2016Article
- Article
- Tumor necrosis factor superfamily 14 (LIGHT) controls thymic stromal lymphopoietin to drive pulmonary fibrosis.The Journal of allergy and clinical immunology · 2015Article
- The Tumor Necrosis Factor Superfamily Molecule LIGHT Promotes Keratinocyte Activity and Skin Fibrosis.The Journal of investigative dermatology · 2015Article
- Increased Serum Levels of LIGHT/TNFSF14 in Nonalcoholic Fatty Liver Disease: Possible Role in Hepatic Inflammation.Clinical and translational gastroenterology · 2015Article
- Immune Response in Hepatitis B Virus Infection.Cold Spring Harbor perspectives in medicine · 2015Review
- Therapeutic blockade of LIGHT interaction with herpesvirus entry mediator and lymphotoxin β receptor attenuates in vivo cytotoxic allogeneic responses.Transplantation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
LIGHT is an important costimulatory molecule for T cell immunity. Recent studies have further implicated its role in innate immunity and inflammatory diseases, but its cellular and molecular mechanisms remain elusive. We report here that LIGHT is upregulated and functions as a proinflammatory cytokine in 2 independent experimental hepatitis models, induced by concanavalin A and Listeria monocytogenes. Molecular mutagenesis studies suggest that soluble LIGHT protein produced by cleavage from the cell membrane plays an important role in this effect through the interaction with the lymphotoxin-beta receptor (LTbetaR) but not herpes virus entry mediator. NK1.1+ T cells contribute to the production, but not the cleavage or effector functions, of soluble LIGHT. Importantly, treatment with a mAb that specifically interferes with the LIGHT-LTbetaR interaction protects mice from lethal hepatitis. Our studies thus identify a what we believe to be a novel function of soluble LIGHT in vivo and offer a potential target for therapeutic interventions in hepatic inflammatory diseases.
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Identifiers
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.