首页> 外文期刊>Endothelium: Journal of endothelial cell research >Contrasting effects of long-term treatment with IFN-gamma in endothelial cells: increase in IL-6 secretion versus decrease in IL-8 secretion, NF-kappa B, and AP-1 activation.
【24h】

Contrasting effects of long-term treatment with IFN-gamma in endothelial cells: increase in IL-6 secretion versus decrease in IL-8 secretion, NF-kappa B, and AP-1 activation.

机译:干扰素-γ长期治疗内皮细胞的对比效果:IL-6分泌增加与IL-8分泌减少,NF-κB和AP-1激活减少。

获取原文
获取原文并翻译 | 示例
           

摘要

The benefit of neutrophil exclusion from type 1 T helper cell (TH1) inflammatory processes was demonstrated in clinical studies. Increased recruitment of lymphocytes and monocytes to endothelium and impaired recruitment of polymorphonuclear neutrophils (PMNs) following interferon-gamma (IFN-gamma) treatment were described. The present study demonstrates that a 24 h treatment with IFN-gamma increases interleukin (IL)-6 release but reduces IL-8 secretion of both untreated and of tumor necrosis factor-alpha (TNF-alpha)-stimulated endothelial cells (ECs), favoring the attraction of lymphocytes but not of neutrophils. Alteration of cytokine release was accompanied by reduced basal and TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) and activator protein-1 (AP-1) activity. However, IFN-gamma application neither altered gene expression of both TNF-alpha receptors (p55 and p75) nor cellular density of TNF-alpha receptor-2 (p75). Therefore, immune-modulatory action of IFN-gamma seems to be mediated by signal transduction molecules.
机译:临床研究表明,将中性粒细胞排除在1型T辅助细胞(TH1)炎症过程中的好处。描述了干扰素-γ(IFN-γ)治疗后淋巴细胞和单核细胞向内皮的募集增加以及多形核中性粒细胞(PMN)募集受损。本研究表明,用IFN-γ进行24小时治疗可增加白细胞介素(IL)-6的释放,但可减少未治疗的和肿瘤坏死因子-α(TNF-α)刺激的内皮细胞(EC)的IL-8分泌,有利于吸引淋巴细胞,但不吸引中性粒细胞。细胞因子释放的改变伴随着减少的基础和TNF-α刺激的核因子-κB(NF-κB)和激活蛋白1(AP-1)活性。但是,使用IFN-γ既不会改变TNF-α受体(p55和p75)的基因表达,也不会改变TNF-α受体2(p75)的细胞密度。因此,IFN-γ的免疫调节作用似乎由信号转导分子介导。

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