ArticleThe Journal of experimental medicine2011
Type I interferon is selectively required by dendritic cells for immune rejection of tumors.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04212377 (An Exploratory Study), which is not on this map. Cited by 687 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.
An Exploratory Study: Dendritic Cells for Immunotherapy of Metastatic Endometrial Cancer Patients
Who cites it
687 citing papers in PubMed, 1,038 citations in OpenAlex.
- Trial
- Trial
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- Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury.Nature communications · 2026Article
- Peptidoglycan Suppresses Melanoma Growth in a Murine Model with Local Immune Activation.International journal of molecular sciences · 2026Article
- Immune-pressure redistribution in resistance to PD-1/PD-L1 blockade: mechanisms, biomarkers, and therapeutic design.Molecular cancer · 2026Review
- Antigen presentation requirements for effective cDC1-based cancer immunotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
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- SBRT embedded in low-dose RT plus αPD-1 (immuno-EclipseRT, iERT) elicits CD8Nature communications · 2026Article
- Engineered Lipid Nanoparticles with Promoted Endosomal Escape and R283S-Mediated Stimulator of Interferon Genes (STING) Activation for Pancreatic Cancer Immunotherapy.Pharmaceutics · 2026Article
- Type I interferon signaling in hematopoietic cells impairs neutrophil antibacterial function in the middle ear during viral co-infection.Cell reports. Medicine · 2026Article
- LPAR4 mediates resistance to interferon-induced stress in soft tissue sarcoma.Science advances · 2026Article
- Argonaute 2 drives resistance to immune checkpoint inhibitors in immunorefractory non-small cell lung cancer.PLoS biology · 2026Article
- Immunomodulation of Pancreatic Cancer via Inhibition of SUMOylation and the CD155/TIGIT Pathway.Molecular cancer therapeutics · 2026Article
- Nanovaccines with ferroptosis, necroptosis and STING-activation for synergistic immunotherapy.Journal of experimental & clinical cancer research : CR · 2026Article
- The promises and challenges of neoantigen cancer vaccines.Nature biotechnology · 2026Review
- Targeting immune checkpoint therapy: The role of manganese in tumor immunotherapy.Cancer pathogenesis and therapy · 2026Review
- Oncolytic Virotherapy and Immunogenic Cell Death: Mechanisms, Platforms, and Clinical Translation.Viruses · 2026Review
- STING agonists as antiviral agents.FEBS letters · 2026Review
627 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer immunoediting is the process whereby the immune system suppresses neoplastic growth and shapes tumor immunogenicity. We previously reported that type I interferon (IFN-α/β) plays a central role in this process and that hematopoietic cells represent critical targets of type I IFN's actions. However, the specific cells affected by IFN-α/β and the functional processes that type I IFN induces remain undefined. Herein, we show that type I IFN is required to initiate the antitumor response and that its actions are temporally distinct from IFN-γ during cancer immunoediting. Using mixed bone marrow chimeric mice, we demonstrate that type I IFN sensitivity selectively within the innate immune compartment is essential for tumor-specific T cell priming and tumor elimination. We further show that mice lacking IFNAR1 (IFN-α/β receptor 1) in dendritic cells (DCs; Itgax-Cre(+)Ifnar1(f/f) mice) cannot reject highly immunogenic tumor cells and that CD8α(+) DCs from these mice display defects in antigen cross-presentation to CD8(+) T cells. In contrast, mice depleted of NK cells or mice that lack IFNAR1 in granulocytes and macrophage populations reject these tumors normally. Thus, DCs and specifically CD8α(+) DCs are functionally relevant targets of endogenous type I IFN during lymphocyte-mediated tumor rejection.
Indexed as
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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.