ArticleNature2017
Tumour ischaemia by interferon-γ resembles physiological blood vessel regression.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.
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.
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Who cites it
181 citing papers in PubMed, 259 citations in OpenAlex.
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- The effects of IFNγ on tissue physiology through structural cells.Nature reviews. Immunology · 2026Review
- Dendritic cell redundancy enables priming of anti-tumor CD4Cancer cell · 2026Article
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- A plant vesicle-dendritic cell chimera for enhancing cancer immunotherapy.Nature communications · 2026Article
- The AICL-KLRF1 axis supports CD4-CD8 T cell communication and cytokine competence in pre-exhausted CD8EMBO reports · 2026Article
- Miniature and versatile genome regulation TnpB-ωRNA toolkits facilitate cancer immunotherapy.Nature communications · 2026Article
- Immunotherapy rechallenge after progression in non-small cell lung cancer: A systematic review and network meta-analysis.iScience · 2026Article
- Overcoming T cell tolerance to tumor self-antigens through catch-bond engineering.Science (New York, N.Y.) · 2026Article
- Cytotoxic CD4Signal transduction and targeted therapy · 2026Review
- CD4+ T Cells Mediate MHC-Deficient Tumor Rejection and Endothelial Cell Reprogramming.Cancer immunology research · 2026Article
- A Novel Strategy for Treating Elderly Patients with Advanced Non-Small Cell Lung Cancer: Exploring the Efficacy and Safety of Anlotinib Combined with PD-1/PD-L1 Inhibitors.OncoTargets and therapy · 2026Article
- Recombinant human adenovirus type 5 synergizes with anti-PD-L1 antibody to promote anti-hepatocellular carcinoma effects through multilevel remodeling of the immune microenvironment.Frontiers in immunology · 2026Article
- Distinct T cell functions enable efficient immunoediting and prevent tumor emergence of developing sarcomas.Cancer cell · 2025Article
- Development of therapeutic cancer vaccines based on cancer immunity cycle.Frontiers of medicine · 2025Review
- IFNγ augments TKI efficacy by alleviating protein unfolding stress to promote GSDME-mediated pyroptosis in hepatocellular carcinoma.Cell death & disease · 2025Article
- Fc-optimized anti-CTLA-4 antibodies increase tumor-associated high endothelial venules and sensitize refractory tumors to PD-1 blockade.Cell reports. Medicine · 2025Article
- Enhancing radiotherapy-induced anti-tumor immunity via nanoparticle-mediated STING agonist synergy.Molecular cancer · 2025Review
- Lung Cancer-Intrinsic SOX2 Expression Mediates Resistance to Checkpoint Blockade Therapy by Inducing Treg-Dependent CD8+ T-cell Exclusion.Cancer immunology research · 2025Article
121 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
26 authors at 8 institutions in 3 countries.
Funding
Abstract
The relative contribution of the effector molecules produced by T cells to tumour rejection is unclear, but interferon-γ (IFNγ) is critical in most of the analysed models. Although IFNγ can impede tumour growth by acting directly on cancer cells, it must also act on the tumour stroma for effective rejection of large, established tumours. However, which stroma cells respond to IFNγ and by which mechanism IFNγ contributes to tumour rejection through stromal targeting have remained unknown. Here we use a model of IFNγ induction and an IFNγ-GFP fusion protein in large, vascularized tumours growing in mice that express the IFNγ receptor exclusively in defined cell types. Responsiveness to IFNγ by myeloid cells and other haematopoietic cells, including T cells or fibroblasts, was not sufficient for IFNγ-induced tumour regression, whereas responsiveness of endothelial cells to IFNγ was necessary and sufficient. Intravital microscopy revealed IFNγ-induced regression of the tumour vasculature, resulting in arrest of blood flow and subsequent collapse of tumours, similar to non-haemorrhagic necrosis in ischaemia and unlike haemorrhagic necrosis induced by tumour necrosis factor. The early events of IFNγ-induced tumour ischaemia resemble non-apoptotic blood vessel regression during development, wound healing or IFNγ-mediated, pregnancy-induced remodelling of uterine arteries. A better mechanistic understanding of how solid tumours are rejected may aid the design of more effective protocols for adoptive T-cell therapy.
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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.