Porcine reproductive and respiratory syndrome virus (PRRSV) up-regulates IL-15 through PKC beta 1-TAK1-NF-kappa B signaling pathway
文献类型: 外文期刊
第一作者: Du, Li
作者: Du, Li;Liu, Yihao;Du, Yinping;Wang, Honglei;Feng, Wen-Hai;Du, Li;Liu, Yihao;Du, Yinping;Wang, Honglei;Du, Yijun;Feng, Wen-Hai;Zhang, Meijie;Du, Yijun
作者机构:
关键词: PRRSV;IL-15;PKC beta 1;NF-kappa B;TAK1
期刊名称:VIROLOGY ( 影响因子:3.616; 五年影响因子:3.967 )
ISSN:
年卷期:
页码:
收录情况: SCI
摘要: Porcine reproductive and respiratory syndrome (PRRS) caused by PRRS virus (PRRSV) is one of the most important infectious diseases in swine industry. IL-15 is a pleiotropic cytokine and has been shown to be essential to transform NKs, CD8 T cells, and other cells of the immune systems into functional effectors. Here, we demonstrated that the broad-spectrum or conventional PKC inhibitors repressed PRRSV-induced IL-15 expression and NF-kappa B activation. Subsequently, we found that the PKC beta specific inhibitor inhibited PRRSV-induced IL-15 production, which was also confirmed by knock-down of PKC beta 1, suggesting that PKC beta 1 is involved in the PRRSV-induced IL-15 expression. In addition, we demonstrated that PRRSV activated NF-kappa B through PKC beta 1-induced TAK1 activation. Finally, we demonstrated that PRRSV activated PKC beta 1 dependent on the participation of TRIF and MAVS. These data indicate that PRRSV up-regulates IL-15 through TRIF/MAVS-PKC beta 1-TAK1-NF-kappa B signaling pathway. These findings will provide new insights into the molecular mechanisms of IL-15 production induced by PRRSV. (C) 2016 Published by Elsevier Inc.
分类号: R37
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