ArticleClinical and experimental immunology2004
Blocking lymphotoxin-beta receptor activation diminishes inflammation via reduced mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expression and leucocyte margination in chronic DSS-induced colitis.
Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 63 citations in OpenAlex.
- Depletion of IgG-producing plasma cells in the colon by treatment of proteasome inhibitor ameliorates chronic DSS-induced colitis in mice.Scientific reports · 2026Article
- Lymphotoxin beta receptorInfection and immunity · 2025Article
- TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/TXNIP/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways.Inflammation · 2025Article
- Gastrointestinal Symptom Cluster is Associated With Epigenetic Regulation of Lymphotoxin Beta in Oncology Patients Receiving Chemotherapy.Biological research for nursing · 2023Article
- DSS-induced colitis activates the kynurenine pathway in serum and brain by affecting IDO-1 and gut microbiota.Frontiers in immunology · 2022Article
- An epithelialProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Metabolic activation and colitis pathogenesis is prevented by lymphotoxin β receptor expression in neutrophils.Mucosal immunology · 2021Article
- The association of lymphotoxin-beta receptor with the subsequent diagnosis of incident gastrointestinal cancer: results from the Dallas Heart Study.Journal of gastrointestinal oncology · 2020Article
- Role of MAdCAM-1-Expressing High Endothelial Venule-Like Vessels in Colitis Induced in Mice Lacking Sulfotransferases Catalyzing L-Selectin Ligand Biosynthesis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Article
- Expression of the novel adipokine C1qTNF-related protein 4 (CTRP4) suppresses colitis and colitis-associated colorectal cancer in mice.Cellular & molecular immunology · 2016Article
- Chemerin aggravates DSS-induced colitis by suppressing M2 macrophage polarization.Cellular & molecular immunology · 2014Article
- Article
- Regulation of inflammation, autoimmunity, and infection immunity by HVEM-BTLA signaling.Journal of leukocyte biology · 2011Review
- Role of TNFR-related 2 mediated immune responses in dextran sulfate sodium-induced inflammatory bowel disease.Molecules and cells · 2011Article
- Effect of α4β7 blockade on intestinal lymphocyte subsets and lymphoid tissue development.Inflammatory bowel diseases · 2010Article
- Anti-adhesion molecule therapy for inflammatory bowel disease.Therapeutic advances in gastroenterology · 2010Article
- Neutralization of LIGHT ameliorates acute dextran sodium sulphate-induced intestinal inflammation.Immunology · 2009Article
- Regulating the mucosal immune system: the contrasting roles of LIGHT, HVEM, and their various partners.Seminars in immunopathology · 2009Review
- Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta.International journal of medical sciences · 2009Article
- Alpha4beta7/MAdCAM-1 interactions play an essential role in transitioning cryptopatches into isolated lymphoid follicles and a nonessential role in cryptopatch formation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lymphotoxin-beta receptor (LTbetaR) pathway is critical for maintenance of organized lymphoid structures and is involved in the development of colitis. To investigate the mechanisms by which LTbetaR activation contributes to the pathology of chronic inflammation we used a soluble LTbetaR-Ig fusion protein as a competitive inhibitor of LTbetaR activation in the mouse model of chronic colitis induced by oral administration of dextran sulphate sodium. Strong expression of LTbeta which constitutes part of the LTalpha(1)beta(2) ligand complex was detected in colonic tissue of mice with chronic colitis. Treatment with LTbetaR-Ig significantly attenuated the development and histological manifestations of the chronic inflammation and reduced the production of inflammatory cytokines such as TNF, IL-1beta, and IL-6. Moreover, LTbetaR-Ig treatment significantly down-regulated mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expression, leading to reduced leucocyte rolling and sticking in postcapillary and collecting venules and reduced extravasation into the intestinal mucosa as quantified by in vivo fluorescence microscopy. Thus, LTbetaR pathway inhibition ameliorates DSS-induced experimental chronic colitis in mice by MAdCAM-1 down-regulation entailing reduced lymphocyte margination and extravasation into the inflamed mucosa. Therefore, a combined treatment with reagents blocking T cell-mediated perpetuation of chronic inflammation such as LTbetaR-Ig together with direct anti-inflammatory reagents such as TNF inhibitors could constitute a promising treatment strategy for chronic colitis.
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