Trial reportThe Journal of clinical investigation2019
IFN-γ drives inflammatory bowel disease pathogenesis through VE-cadherin-directed vascular barrier disruption.
Trial report in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 3 of them syntheses that pooled it.
What it found
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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.
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
158 citing papers in PubMed, 3 syntheses or guidelines pooled it, 241 citations in OpenAlex.
- Efficacy and safety of imatinib in patients with COVID-19: a systematic review and meta-analysis.Wiener klinische Wochenschrift · 2025Pooled it
- The Association between Genetics and Response to Treatment with Biologics in Patients with Psoriasis, Psoriatic Arthritis, Rheumatoid Arthritis, and Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Systematic Review and Meta-analysis of Peripheral Blood DNA Methylation Studies in Inflammatory Bowel Disease.Journal of Crohn's & colitis · 2023Pooled it
- Article
- Targeting the FOXP3-T-bet interaction to restore Treg stability in IFN-γ-driven autoimmunity.Cellular & molecular immunology · 2026Article
- NKRInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Effects of Common Food Additives Kappa-, Iota- and Lambda-Carrageenans on Intestinal Epithelial Cell Activation and Barrier Disruption.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- Ex Vivo Human Colonic Explants Identify Metabolic Alterations and Cytokine Dysregulation in Ulcerative Colitis: A Pilot Study.Digestive diseases and sciences · 2026Article
- Off‑the‑shelf, engineered non-living stem cell strategy for advancing cellular therapies.Nature biomedical engineering · 2026Article
- In vitro modeling of inflammatory bowel diseases using a newly developed immunocompetent colon epithelial monolayer co-culture model.npj biomedical innovations · 2026Article
- Histologic signatures as predictors of intestinal barrier impairment in inflammatory bowel disease: integration with endoscopic and molecular markers.Journal of Crohn's & colitis · 2026Article
- PRMT5/Sohlh2/Sirt1 Signaling Pathway in Vascular Endothelial Cells Modulates Lung Metastasis of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ST8Sia6-dependent glycosylation restrains gut inflammation and pathogenic TCell reports · 2026Article
- Evaluation of the Anti-Inflammatory Activity of Selected Plant Extracts in an In Vitro Model of Inflammation Using LPS-Stimulated Macrophages.Biomedicines · 2026Article
- Crosstalk between inflammation and autophagy in CeD organoids.Scientific reports · 2026Article
- Recombinant BMP9 Reinforces Gut Vascular Barrier in Experimental Colitis.Biomedicines · 2026Article
- CU104, a novel barrier function enhancer, improves colitis via modulation of barrier function and immune cell recruitment.Frontiers in immunology · 2026Article
- Second-order regulation: IFN-γ suppresses IL-17A-mediated type 3 inflammation.Frontiers in immunology · 2026Article
- Microbiota-specific serum IgG links gut and joints through immune-endothelial crosstalk in arthritis.Frontiers in microbiology · 2026Article
- Gegen Qinlian decoction alleviates DSS-induced colitis in mice through coordinated modulation of gut microbiota, serum metabolome, and colonic γδT cell responses.Frontiers in immunology · 2026Article
98 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
24 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder with rising incidence. Diseased tissues are heavily vascularized. Surprisingly, the pathogenic impact of the vasculature in IBD and the underlying regulatory mechanisms remain largely unknown. IFN-γ is a major cytokine in IBD pathogenesis, but in the context of the disease, it is almost exclusively its immune-modulatory and epithelial cell-directed functions that have been considered. Recent studies by our group demonstrated that IFN-γ also exerts potent effects on blood vessels. Based on these considerations, we analyzed the vessel-directed pathogenic functions of IFN-γ and found that it drives IBD pathogenesis through vascular barrier disruption. Specifically, we show that inhibition of the IFN-γ response in vessels by endothelial-specific knockout of IFN-γ receptor 2 ameliorates experimentally induced colitis in mice. IFN-γ acts pathogenic by causing a breakdown of the vascular barrier through disruption of the adherens junction protein VE-cadherin. Notably, intestinal vascular barrier dysfunction was also confirmed in human IBD patients, supporting the clinical relevance of our findings. Treatment with imatinib restored VE-cadherin/adherens junctions, inhibited vascular permeability, and significantly reduced colonic inflammation in experimental colitis. Our findings inaugurate the pathogenic impact of IFN-γ-mediated intestinal vessel activation in IBD and open new avenues for vascular-directed treatment of this disease.
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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.