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

Tyler C. Moore, Phyllis M. Kumm, Deborah M Brown, Thomas M Petro

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)122-128
Number of pages7
JournalCancer Letters
Volume346
Issue number1
DOIs
StatePublished - Apr 28 2014

Fingerprint

Poly I-C
Experimental Melanomas
Natural Killer Cells
Interferons
Growth
Granzymes
Interleukin-15
Therapeutic Uses
Virus Diseases
Interleukin-12
Knockout Mice
Dendritic Cells
Melanoma
Interleukin-6
Macrophages
Therapeutics
Neoplasms

Keywords

  • Cytokines
  • IRF3
  • Melanoma
  • NK-cells
  • Poly-I:C

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Interferon response factor 3 is crucial to poly-I : C induced NK cell activity and control of B16 melanoma growth. / Moore, Tyler C.; Kumm, Phyllis M.; Brown, Deborah M; Petro, Thomas M.

In: Cancer Letters, Vol. 346, No. 1, 28.04.2014, p. 122-128.

Research output: Contribution to journalArticle

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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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