ArticleFrontiers in immunology2018
The Tumor Necrosis Factor Superfamily Members TNFSF14 (LIGHT), Lymphotoxin β and Lymphotoxin β Receptor Interact to Regulate Intestinal Inflammation.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- eQTL in diseased colon tissue identifies potential target genes associated with IBD.Nature communications · 2026Article
- A bioactive soluble recombinant mouse LIGHT promotes effective tumor immune cell infiltration delaying tumor growth.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Spatial transcriptomics delineates potential differences in intestinal phenotypes of cardiac and classical necrotizing enterocolitis.iScience · 2025Article
- TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD.Frontiers in immunology · 2025Review
- The Cellular and Transcriptomic Early Innate Immune Response to BCG Vaccination in Mice.Cells · 2024Article
- Tumor Necrosis Factor Superfamily 14 Regulates the Inflammatory Response of Human Dental Pulp Stem Cells.Current issues in molecular biology · 2024Article
- LTβR-RelB signaling in intestinal epithelial cells protects from chemotherapy-induced mucosal damage.Frontiers in immunology · 2024Article
- Development and validation a prognostic model based on natural killer T cells marker genes for predicting prognosis and characterizing immune status in glioblastoma through integrated analysis of single-cell and bulk RNA sequencing.Functional & integrative genomics · 2023Article
- Costimulatory molecule expression profile as a biomarker to predict prognosis and chemotherapy response for patients with small cell lung cancer.Cancer immunology, immunotherapy : CII · 2023Article
- The soluble VCAM-1 level is a potential biomarker predicting severe acute graft versus host disease after allogeneic hematopoietic cell transplantation.BMC cancer · 2022Article
- Realigning the LIGHT signaling network to control dysregulated inflammation.The Journal of experimental medicine · 2022Article
- Article
- CD4Frontiers in immunology · 2022Article
- Mechanisms for the Invasion and Dissemination ofThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2022Review
- Construction and Validation of a Novel Immune Checkpoint-Related Model in Clear Cell Renal Cell Carcinoma.Disease markers · 2022Article
- HVEM structures and mutants reveal distinct functions of binding to LIGHT and BTLA/CD160.The Journal of experimental medicine · 2021Article
- Recent Advances in Glioma Therapy: Combining Vascular Normalization and Immune Checkpoint Blockade.Cancers · 2021Review
- Metabolic activation and colitis pathogenesis is prevented by lymphotoxin β receptor expression in neutrophils.Mucosal immunology · 2021Article
- Tumor Necrosis Factor Family Member Profile Predicts Prognosis and Adjuvant Chemotherapy Benefit for Patients With Small-Cell Lung Cancer.Frontiers in immunology · 2021Article
- Unraveling the Role of Immune Checkpoints in Leishmaniasis.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Over 1.5 million individuals in the United States are afflicted with inflammatory bowel disease (IBD). While the progression of IBD is multifactorial, chronic, unresolved inflammation certainly plays a key role. Additionally, while multiple immune mediators have been shown to affect pathogenesis, a comprehensive understanding of disease progression is lacking. Previous work has demonstrated that a member of the TNF superfamily, TNFSF14 (LIGHT), which is pro-inflammatory in several contexts, surprisingly plays an important role in protection from inflammation in mouse models of colitis, with LIGHT deficient mice having more severe disease pathogenesis. However, LIGHT is a single member of a complex signaling network. It signals through multiple receptors, including herpes virus entry mediator (HVEM) and lymphotoxin beta receptor (LTβR); these two receptors in turn can bind to other ligands. It remains unknown which receptors and competing ligands can mediate or counteract the outcome of LIGHT-signaling during colitis. Here we demonstrate that LIGHT signaling through LTβR, rather than HVEM, plays a critical role in the progression of DSS-induced colitis, as LTβR deficient mice exhibit a more severe disease phenotype. Further, mice deficient in LTαβ do not exhibit differential colitis progression compared to WT mice. However, deletion of both LIGHT and LTαβ, but not deletion of both LTαβ and LTβR, resulted in a reversal of the adverse effects associated with the loss of LIGHT. In sum, the LIGHT/LTαβ/LTβR signaling network contributes to DSS colitis, but there may be additional receptors or indirect effects, and therefore, the relationships between these receptors and ligands remains enigmatic.
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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.