ArticleCancer letters2014
Interferon response factor 3 is crucial to poly-I:C induced NK cell activity and control of B16 melanoma growth.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
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- PLP2 Could Be a Prognostic Biomarker and Potential Treatment Target in Glioblastoma Multiforme.Pharmacogenomics and personalized medicine · 2023Article
- Ovalbumin and Poly(i:c) Encapsulated Dendritic Cell-Targeted Nanoparticles for Immune Activation in the Small Intestinal Lymphatic System.Advanced healthcare materials · 2022Article
- PD-L1 overexpression in EBV-positive gastric cancer is caused by unique genomic or epigenomic mechanisms.Scientific reports · 2021Article
- Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ.Immunobiology · 2019Article
- Cryo-thermal therapy induces macrophage polarization for durable anti-tumor immunity.Cell death & disease · 2019Article
- Activation of IRF3 contributes to IFN-γ and ISG54 expression during the immune responses to B16F10 tumor growth.International immunopharmacology · 2017Article
- The cryo-thermal therapy eradicated melanoma in mice by eliciting CD4Cell death & disease · 2017Article
- Significant role for IRF3 in both T cell and APC effector functions during T cell responses.Cellular immunology · 2016Article
- TLR-3 stimulation improves anti-tumor immunity elicited by dendritic cell exosome-based vaccines in a murine model of melanoma.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Interferon Response Factor 3 (IRF3) induces several NK-cell activating factors, is activated by poly-I:C, an experimental cancer therapeutic, but is suppressed during many viral infections. IRF3 Knockout (KO) mice exhibited enhanced B16 melanoma growth, impaired intratumoral NK cell infiltration, but not an impaired poly-I:C therapeutic effect due to direct suppression of B16 growth. IRF3 was responsible for poly-I:C decrease in TIM-3 expression by intratumoral dendritic cells, induction of NK-cell Granzyme B and IFN-γ, and induction of macrophage IL-12, IL-15, IL-6, and IRF3-dependent NK-activating molecule (INAM). Thus, IRF3 is a key factor controlling melanoma growth through NK-cell activities, especially during poly-I:C therapy.
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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.