...
首页> 外文期刊>Cytokine >CCL20 produced in the cytokine network of rheumatoid arthritis recruits CCR6+ mononuclear cells and enhances the production of IL-6.
【24h】

CCL20 produced in the cytokine network of rheumatoid arthritis recruits CCR6+ mononuclear cells and enhances the production of IL-6.

机译:在类风湿性关节炎的细胞因子网络中产生的CCL20募集CCR6 +单核细胞并增强IL-6的产生。

获取原文
获取原文并翻译 | 示例
           

摘要

Although a notable amount of CCL20 is detectable in the synovial fluid of human rheumatoid arthritis (RA), its role in the pathogenesis of RA remains to be determined. IL-1beta vigorously induced the production of CCL20 from FLSs of human RA and the production of CCL20 induced by TNF-alpha was partially attributed to a trace amount of IL-1beta induced by TNF-alpha. Although IL-6 failed to induce CCL20, TNF-alpha-induced IL-6 enhanced the production of CCL20 in an autocrine/paracrine manner. To determine the role of CCL20 and its sole receptor CCR6 in the recruitment of mononuclear cells (MNCs) into the inflamed joint of RA, conditioned medium of IL-1beta-stimulated FLSs was used in migration assays. The conditioned medium significantly recruited CCR6(+) MNCs in a CCL20-dependent manner. The production of CCL20 induced by TNF-alpha and IL-1beta was modified by helper-T-cell-derived cytokines. Interestingly, CCL20 enhanced the production of IL-6 coordinately with the stimulation of IL-17 but not with that of IFN-gamma. These findings imply FLSs stimulated by proinflammatory cytokines recruit CCR6(+) MNCs including IL-17-producing-helper T cells into the inflamed joint, leading to the enhancement of the production of CCL20, which chemokine and IL-17 coordinately induce proinflammatory cytokines.
机译:尽管在人类风湿性关节炎(RA)的滑液中可检测到显着量的CCL20,但其在RA发病机理中的作用仍有待确定。 IL-1beta强烈诱导人RA FLS产生CCL20,TNF-α诱导的CCL20产生部分归因于TNF-α诱导的痕量IL-1beta。尽管IL-6未能诱导CCL20,但TNF-α诱导的IL-6以自分泌/旁分泌方式增加了CCL20的产生。为了确定CCL20及其唯一受体CCR6在将单核细胞(MNC)募集到RA的发炎关节中的作用,将IL-1beta刺激的FLSs的条件培养基用于迁移分析。条件培养基以CCL20依赖性方式大量募集CCR6(+)MNC。 TNF-α和IL-1β诱导的CCL20的产生被辅助T细胞衍生的细胞因子修饰。有趣的是,CCL20与IL-17的刺激协同增强了IL-6的产生,但与IFN-γ的刺激却没有。这些发现暗示,由促炎细胞因子刺激的FLS将包括IL-17产生辅助T细胞在内的CCR6(+)MNC募集到发炎的关节中,导致CCL20的产生增加,趋化因子和IL-17协同诱导促炎细胞因子。

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