| First Author | Moore TC | Year | 2014 |
| Journal | Cancer Lett | Volume | 346 |
| Issue | 1 | Pages | 122-8 |
| PubMed ID | 24368188 | Mgi Jnum | J:208168 |
| Mgi Id | MGI:5561190 | Doi | 10.1016/j.canlet.2013.12.022 |
| Citation | Moore TC, et al. (2014) Interferon response factor 3 is crucial to poly-I:C induced NK cell activity and control of B16 melanoma growth. Cancer Lett 346(1):122-8 |
| abstractText | 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-gamma, 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. |
