ArticleClinical and experimental immunology2006
Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice.
Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
217 citing papers in PubMed, 368 citations in OpenAlex.
- The TLR9 Agonist Cobitolimod Induces IL10-Producing Wound Healing Macrophages and Regulatory T Cells in Ulcerative Colitis.Journal of Crohn's & colitis · 2020Trial
- IFN-γ drives inflammatory bowel disease pathogenesis through VE-cadherin-directed vascular barrier disruption.The Journal of clinical investigation · 2019Trial
- Trial
- Targeting the FOXP3-T-bet interaction to restore Treg stability in IFN-γ-driven autoimmunity.Cellular & molecular immunology · 2026Article
- Inducible cAMP Early Repressor Limits Glycolytic Programming in Regulatory T Cells and Supports Control of Inflammatory Colitis.European journal of immunology · 2026Article
- OTUD5 maintains STAT1/2 stability and promotes IFNγ-driven intestinal inflammation.The Journal of biological chemistry · 2026Article
- Macrophages tune NK cell IFNγ production through direct lipid transfer.Nature communications · 2026Article
- Epithelial TRIM27 Inhibits Intestinal Inflammation in Ulcerative Colitis by the USP7/TRIM27-IKK Double Negative-Feedback.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- An HHEX/IKKα positive feedback loop promotes intestinal inflammation.The Journal of clinical investigation · 2026Article
- The roles and heterogeneity of CD8International journal of molecular medicine · 2026Review
- Dexpramipexole alleviates chronic allodynia from sciatic neuropathy and reduces spinal interferon-γ and other proinflammatory cytokines in spinal cord and dorsal root ganglia in mice.Medical research archives · 2026Article
- Analysis of the use of monoclonal antibodies in the treatment of Crohn's disease.Antibody therapeutics · 2026Review
- ILC plasticity in intestinal immune barrier remodeling: current evidence and therapeutic implications for inflammatory bowel disease.Frontiers in immunology · 2026Review
- Crotoxin fromFrontiers in immunology · 2026Article
- Tissue-adapted Tregs harness inflammatory signals to promote intestinal repair from therapy-related injury.Signal transduction and targeted therapy · 2025Article
- E. coli-activated cellular circuit restrains intestinal inflammatory microbiota-specific T cells and protects against colitis.Cell reports · 2025Article
- A loss-of-function human ADAR variant activates innate immune response and promotes bowel inflammation.Nature communications · 2025Article
- Mucosal Responses to Type II Interferon in IBD.Inflammatory bowel diseases · 2025Article
- Combining mucosal microbiome and host multi-omics data shows prognostic potential in paediatric ulcerative colitis.Nature communications · 2025Article
- Article
157 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokines may be crucially involved in the pathogenesis of inflammatory bowel diseases (IBD), but it remains controversial whether interferon (IFN)-gamma, a typical proinflammatory cytokine, is an essential mediator to cause the disorders. In the present study, IFN-gamma(-/-) and wild-type (WT) C57BL/6 mice were fed 2.5% dextran sodium sulphate (DSS) in drinking water for 7 days, in order to investigate DSS-induced intestinal inflammation. The DSS-treated WT mice exhibited a robust production of IFN-gamma in the gut, a remarkable loss of body weight, as well as high rate of mortality (60%). In striking contrast, IFN-gamma deficient mice did not develop DSS-induced colitis, as indicated by the maintenance of body weight and survival rate of 100%. Severe intestinal inflammation was demonstrated exclusively in WT animals in terms of the shortening of the bowel as well as the elevation of the disease activity index, myeloperoxidase (MPO) activity and serum haptoglobin level. Histological study of DSS-treated WT intestine revealed disruption of mucosal epithelium and massive infiltration of inflammatory cells, while the organ from IFN-gamma(-/-) mice remained virtually normal in appearance. Enzyme-linked immunosorbent assay (ELISA) analyses indicated abundant production of three chemokines, i.e. monokine induced by interferon-gamma (MIG), interferon-inducible protein 10 (IP-10) and monocyte chemoattractant protein-1 (MCP-1), in the DSS-irritated intestine of WT but not of IFN-gamma(-/-) mice. The present results demonstrate clearly that IFN-gamma plays indispensable roles in the initiation of DSS colitis, and some chemokines are produced in an IFN-gamma-dependent fashion.
Indexed as
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.