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

doi:10.1016/j.canlet.2013.12.022

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 journal › Article › peer-review

17 Scopus citations

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 language	English (US)
Pages (from-to)	122-128
Number of pages	7
Journal	Cancer Letters
Volume	346
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2013.12.022
State	Published - Apr 28 2014

Keywords

Cytokines
IRF3
Melanoma
NK-cells
Poly-I:C

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1016/j.canlet.2013.12.022

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

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.",

keywords = "Cytokines, IRF3, Melanoma, NK-cells, Poly-I:C",

author = "Moore, {Tyler C.} and Kumm, {Phyllis M.} and Brown, {Deborah M.} and Petro, {Thomas M.}",

note = "Funding Information: The authors wish to thank Marian Schmid for her excellent animal care and animal technical services. This work was supported by funding from the University of Nebraska Medical Center College of Dentistry and University of Nebraska Lincoln, School of Biological Sciences, and supported by Award Number P30GM10350903 and P20GM103489 from the National Institute of General Medicine, a component of the National Institutes of Health (NIH). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.",

year = "2014",

month = apr,

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doi = "10.1016/j.canlet.2013.12.022",

language = "English (US)",

volume = "346",

pages = "122--128",

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T2 - C induced NK cell activity and control of B16 melanoma growth

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AU - Kumm, Phyllis M.

AU - Brown, Deborah M.

AU - Petro, Thomas M.

N1 - Funding Information: The authors wish to thank Marian Schmid for her excellent animal care and animal technical services. This work was supported by funding from the University of Nebraska Medical Center College of Dentistry and University of Nebraska Lincoln, School of Biological Sciences, and supported by Award Number P30GM10350903 and P20GM103489 from the National Institute of General Medicine, a component of the National Institutes of Health (NIH). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health.

PY - 2014/4/28

Y1 - 2014/4/28

N2 - 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.

AB - 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.

KW - Cytokines

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KW - NK-cells

KW - Poly-I:C

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

Abstract

Keywords

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