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

Interferon response factor 3 is crucial to poly-I:C induced NK cell activity and control of B16 melanoma growth.
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干扰素反应因子 3 对于多聚 I:C 诱导的 NK 细胞活性和控制 B16 黑色素瘤生长至关重要。

DOI:
10.1016/j.canlet.2013.12.022
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发表时间:
2014-04-28
期刊:
影响因子:
9.7
通讯作者:
Petro, Thomas M.
Petro, Thomas M.
中科院分区:
医学1区
文献类型:
--
作者:
Moore, Tyler C.;Kumm, Phyllis M.;Brown, Deborah M.;Petro, Thomas M.

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干扰素应答因子3(IRF 3)诱导几种NK细胞活化因子,被实验性癌症治疗剂poly-I:C活化,但在许多病毒感染期间被抑制。IRF 3敲除(KO)小鼠表现出B16黑色素瘤生长增强,瘤内NK细胞浸润受损,但由于B16生长的直接抑制,聚I:C治疗效果未受损。IRF 3负责肿瘤内树突状细胞的TIM-3表达中poly-I:C的减少,NK细胞颗粒酶B和IFN-γ的诱导,以及巨噬细胞IL-12、IL-15、IL-6和IRF 3依赖性NK活化分子(INAM)的诱导。因此,IRF 3是通过NK细胞活性控制黑色素瘤生长的关键因子,特别是在聚I:C治疗期间。
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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