...
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >p38 activation through Toll-like receptors modulates IFN-?3-induced expression of the Tap-1 gene only in macrophages
【24h】

p38 activation through Toll-like receptors modulates IFN-?3-induced expression of the Tap-1 gene only in macrophages

机译:通过Toll样受体的p38激活仅在巨噬细胞中调节IFN-α3诱导的Tap-1基因的表达

获取原文
           

摘要

Although interferon-?3 (IFN-?3) induces the transporter associated with antigen processing (Tap)-1 expression in macrophages, cooperation with lipopolysaccharide signaling through Toll-like receptor 4 (TLR4) accelerates the kinetics and increases the overall levels of this gene. In this report, we show that peptidoglycan signaling through TLR2 and bacterial CpG DNA signaling through TLR9 are functionally equivalent at synergizing with IFN-?3 in regulating Tap-1 expression in macrophages. Activation of the p38 mitogen-activated protein kinase is necessary for this response, which correlates with increased phosphorylation of signal transducer and activator of transcription-1 on serine 727. Activation of p38, however, is not sufficient, as this signaling event does not affect the response to IFN-?3 in HeLa cells. The cooperation between these different signaling pathways also requires membrane fluidity. These data suggest that macrophages possess an ability to coordinate the signaling between the IFN-?3 and TLR receptors.
机译:尽管干扰素-α3(IFN-α3)诱导了巨噬细胞中与抗原加工(Tap)-1表达相关的转运蛋白,但与通过Toll样受体4(TLR4)的脂多糖信号传导的协同作用加快了动力学并提高了其总体水平基因。在本报告中,我们显示了通过TLR2进行的肽聚糖信号传导和通过TLR9进行的细菌CpG DNA信号传导在调节IFN-γ3巨噬细胞中Tap-1表达方面的功能相同。 p38丝裂原激活的蛋白激酶的激活对于此反应是必需的,这与信号转导子和丝氨酸727上转录1激活子的磷酸化增加有关。但是,p38激活是不够的,因为此信号转导事件不会影响HeLa细胞对IFN-α3的反应。这些不同信号通路之间的合作也需要膜流动性。这些数据表明巨噬细胞具有协调IFN-β3和TLR受体之间的信号传导的能力。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号