Literature DB >> 24368188

Interferon response factor 3 is crucial to poly-I:C induced NK cell activity and control of B16 melanoma growth.

Tyler C Moore1, Phyllis M Kumm2, Deborah M Brown3, Thomas M Petro4.   

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.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Cytokines; IRF3; Melanoma; NK-cells; Poly-I:C

Mesh：

Substances：

Year:  2013        PMID： 24368188      PMCID： PMC3963264          DOI： 10.1016/j.canlet.2013.12.022

Source DB:  PubMed          Journal:  Cancer Lett        ISSN： 0304-3835            Impact factor:   8.679


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