ArticleThe Journal of experimental medicine1999
Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2(-/-) mice upon transfer of CD4(+)CD45RB(hi) T cells.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 125 citations in OpenAlex.
- The Relevance of Experimental Models in Assessing the Impact of Oxidative Stress on Intestinal Pathology.Journal of clinical medicine · 2025Review
- Human Amniotic Epithelial Stem Cells Promote Colonic Recovery in Experimental Colitis via Exosomal MiR-23a-TNFR1-NF-κB Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- Anti-Inflammatory Effect of Topiramate in a Chronic Model of TNBS-Induced Colitis.International journal of molecular sciences · 2022Article
- TNF hampers intestinal tissue repair in colitis by restricting IL-22 bioavailability.Mucosal immunology · 2022Article
- The dichotomous outcomes of TNFα signaling in CD4Frontiers in immunology · 2022Review
- An Update of Research Animal Models of Inflammatory Bowel Disease.TheScientificWorldJournal · 2021Review
- The many faces of tumor necrosis factor signaling in the intestinal epithelium.Genes and immunity · 2019Review
- The orphan nuclear receptor LRH-1/NR5a2 critically regulates T cell functions.Science advances · 2019Article
- A New Venue of TNF Targeting.International journal of molecular sciences · 2018Review
- Divergent Roles of Interferon-γ and Innate Lymphoid Cells in Innate and Adaptive Immune Cell-Mediated Intestinal Inflammation.Frontiers in immunology · 2018Article
- Hemin reduces inflammation associated with TNBS-induced colitis.Clinical and experimental gastroenterology · 2018Article
- TNFα deficiency results in increased IL-1β in an early onset of spontaneous murine colitis.Cell death & disease · 2017Article
- T-bet expression by Th cells promotes type 1 inflammation but is dispensable for colitis.Mucosal immunology · 2016Article
- Early Detection of T cell Transfer-induced Autoimmune Colitis by In Vivo Imaging System.Scientific reports · 2016Article
- CD4 T cells are required for both development and maintenance of disease in a new mouse model of reversible colitis.Mucosal immunology · 2016Article
- TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance.PLoS pathogens · 2014Article
- Bifidobacterium lactis attenuates onset of inflammation in a murine model of colitis.World journal of gastroenterology · 2011Article
- Stem cells as potential therapeutic targets for inflammatory bowel disease.Frontiers in bioscience (Scholar edition) · 2010Review
- TNF suppresses acute intestinal inflammation by inducing local glucocorticoid synthesis.The Journal of experimental medicine · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we addressed the role of tumor necrosis factor (TNF)-alpha and lymphotoxin (LT)-alpha in the development of colitis and defined the cellular sources (T cells versus non-T cells) of TNF (TNF-alpha and LT-alpha) relevant to disease development. After adoptive transfer of TNF(+/+) CD4(+)CD45RB(hi) splenocytes into TNF(+/+) recombination activating gene (RAG)2(-/-) mice, the recipients develop massive inflammation of the large intestinal mucosa concurrent with massive weight loss. In contrast, clinical signs of disease are completely absent in TNF(-/-)RAG2(-/-) recipients of TNF(-/-) CD4(+)CD45RB(hi) T cells, although elevated numbers of interferon-gamma-producing cells are present in the colonic mucosa. Surprisingly, upon transfer of TNF(-/-)CD4(+)CD45RB(hi) T cells into TNF(+/+)RAG2(-/-) recipients, colitis develops with kinetics similar to those upon transfer of TNF(+/+)CD4(+)CD45RB(hi) donor cells. In contrast, no clinical signs of colitis are observed in TNF(-/-)RAG2(-/-) recipients of TNF(+/+)CD4(+)CD45RB(hi) T cells. This protection from colitis is not a consequence of the absence of LT-alpha, as TNF-alpha(-/-)RAG2(-/-) recipients of TNF-alpha(-/-) CD4(+)CD45RB(hi) T cells are also protected from colitis induction. These results demonstrate the importance of TNF production by non-T cells of the colonic mucosa in the pathogenesis of colitis and provide direct evidence for a nonredundant role of TNF-alpha in this mouse model of colitis.
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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.