ArticleArthritis & rheumatology (Hoboken, N.J.)2014
Regulation of early cartilage destruction in inflammatory arthritis by death receptor 3.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Therapeutic Potential of Tulisokibart and Anti-TL1A Therapy in Inflammatory Disorders: Current Insights and Future Directions.Clinical reviews in allergy & immunology · 2026Review
- The Therapeutic Potential of Targeting TL1A in a Spectrum of Inflammatory Disorders.Journal of inflammation research · 2026Review
- Functions of Macrophages, T Cells, and Neutrophils in the Synovial Microenvironment of Osteoarthritis.Journal of inflammation research · 2025Review
- Starvation and Inflammation Modulate Adipose Mesenchymal Stromal Cells' Molecular Signature.Journal of personalized medicine · 2024Article
- Roles of tumor necrosis factor-like ligand 1A in γδT-cell activation and psoriasis pathogenesis.Frontiers in immunology · 2024Article
- Article
- Collagenase-Induced Mouse Model of Osteoarthritis-A Thorough Flow Cytometry Analysis.Life (Basel, Switzerland) · 2022Article
- Role of TL1A in Inflammatory Autoimmune Diseases: A Comprehensive Review.Frontiers in immunology · 2022Review
- Proinflammatory T cell polarization is already present in patients with early knee osteoarthritis.Arthritis research & therapy · 2021Article
- TL1A (TNFSF15) and DR3 (TNFRSF25): A Co-stimulatory System of Cytokines With Diverse Functions in Gut Mucosal Immunity.Frontiers in immunology · 2019Review
- Death Receptor 3 regulates distinct pathological attributes of acute versus chronic murine allergic lung inflammation.Cellular immunology · 2017Article
- Matrine derivate MASM uncovers a novel function for ribosomal protein S5 in osteoclastogenesis and postmenopausal osteoporosis.Cell death & disease · 2017Article
- Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases.Nature reviews. Rheumatology · 2017Review
- Article
- Immunology of Gut-Bone Signaling.Advances in experimental medicine and biology · 2017Article
- Review: Novel Insights Into Tumor Necrosis Factor Receptor, Death Receptor 3, and Progranulin Pathways in Arthritis and Bone Remodeling.Arthritis & rheumatology (Hoboken, N.J.) · 2016Review
- Death Receptor 3 Promotes Chemokine-Directed Leukocyte Recruitment in Acute Resolving Inflammation and Is Essential for Pathological Development of Mesothelial Fibrosis in Chronic Disease.The American journal of pathology · 2016Article
- Characterization of death receptor 3-dependent aortic changes during inflammatory arthritis.Pharmacology research & perspectives · 2016Article
- The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.Journal of leukocyte biology · 2015Review
- Death Receptor 3 (TNFRSF25) Increases Mineral Apposition by Osteoblasts and Region Specific New Bone Formation in the Axial Skeleton of Male DBA/1 Mice.Journal of immunology research · 2015Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate the role of death receptor 3 (DR-3) and its ligand tumor necrosis factor-like molecule 1A (TL1A) in the early stages of inflammatory arthritis.
methodsAntigen-induced arthritis (AIA) was generated in C57BL/6 mice deficient in the DR-3 gene (DR3(-/-) ) and their DR3(+/+) (wild-type) littermates by priming and intraarticular injection of methylated bovine serum albumin. The joints were sectioned and analyzed histochemically for damage to cartilage and expression of DR3, TL1A, Ly-6G (a marker for neutrophils), the gelatinase matrix metalloproteinase 9 (MMP-9), the aggrecanase ADAMTS-5, and the neutrophil chemoattractant CXCL1. In vitro production of MMP-9 was measured in cultures from fibroblasts, macrophages, and neutrophils following the addition of TL1A and other proinflammatory stimuli.
resultsDR3 expression was up-regulated in the joints of wild-type mice following generation of AIA. DR3(-/-) mice were protected against cartilage damage compared with wild-type mice, even at early time points prior to the main accumulation of Teff cells in the joint. Early protection against AIA in vivo correlated with reduced levels of MMP-9. In vitro, neutrophils were major producers of MMP-9, while neutrophil numbers were reduced in the joints of DR3(-/-) mice. However, TL1A neither induced MMP-9 release nor affected the survival of neutrophils. Instead, reduced levels of CXCL1 were observed in the joints of DR3(-/-) mice.
conclusionDR-3 drives early cartilage destruction in the AIA model of inflammatory arthritis through the release of CXCL1, maximizing neutrophil recruitment to the joint and leading to enhanced local production of cartilage-destroying enzymes.
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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.