• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>International Journal of Molecular Sciences >C-C Motif Ligand 20 (CCL20) and C-C Motif Chemokine Receptor 6 (CCR6) in Human Peripheral Blood Mononuclear Cells: Dysregulated in Ulcerative Colitis and a Potential Role for CCL20 in IL-1β Release
【2h】

C-C Motif Ligand 20 (CCL20) and C-C Motif Chemokine Receptor 6 (CCR6) in Human Peripheral Blood Mononuclear Cells: Dysregulated in Ulcerative Colitis and a Potential Role for CCL20 in IL-1β Release

机译：人外周血单个核细胞中的C-C母体配体20（CCL20）和C-C母体趋化因子受体6（CCR6）：在溃疡性结肠炎中失调并且CCL20在IL-1β释放中的潜在作用

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The chemokine C-C motif ligand 20 (CCL20) is increased in the colonic mucosa during active inflammatory bowel disease (IBD) and can be found both in the epithelium and immune cells in the lamina propria. The present study investigated CCL20 and C-C motif Chemokine Receptor 6 (CCR6) in peripheral blood mononuclear cells (PBMCs) (n = 40) from IBD patients and healthy controls, to identify inductors of CCL20 release encountered in a local proinflammatory environment. CCL20 release from PBMCs was increased when activating TLR2/1 or NOD2, suggesting that CCL20 is part of a first line response to danger-associated molecular patterns also in immune cells. Overall, ulcerative colitis (UC) had a significantly stronger CCL20 release than Crohn’s disease (CD) (+242%, p < 0.01), indicating that the CCL20-CCR6 axis may be more involved in UC. The CCL20 receptor CCR6 is essential for the chemotactic function of CCL20. UC with active inflammation had significantly decreased CCR6 expression and a reduction in CCR6+ cells in circulation, indicating chemoattraction of CCR6+ cells from circulation towards peripheral tissues. We further examined CCL20 induced release of cytokines from PBMCs. Stimulation with CCL20 combined with TNF increased IL-1β release from PBMCs. By attracting additional immune cells, as well as inducing proinflammatory IL-1β release from immune cells, CCL20 may protract the inflammatory response in ulcerative colitis.
机译：趋化因子C-C基序配体20（CCL20）在活动性炎性肠病（IBD）期间在结肠粘膜中增加，并且可以在固有层的上皮和免疫细胞中发现。本研究调查了来自IBD患者和健康对照者的外周血单核细胞（PBMC）（n = 40）中的CCL20和C-C基序趋化因子受体6（CCR6），以确定在局部促炎性环境中遇到的CCL20释放诱导物。激活TLR2 / 1或NOD2时，PBMC中CCL20的释放增加，表明CCL20是免疫细胞中对危险相关分子模式的一线反应的一部分。总体而言，溃疡性结肠炎（UC）的CCL20释放量比克罗恩病（CD）明显更强（+ 242％，p <0.01），表明CCL20-CCR6轴可能与UC相关。 CCL20受体CCR6对于CCL20的趋化功能至关重要。具有活动性炎症的UC明显降低了循环中CCR6的表达，并减少了CCR6 + 细胞，表明CCR6 + 细胞从循环中向周围组织趋化。我们进一步检查了CCL20诱导的PBMC细胞因子释放。 CCL20与TNF联合刺激可增加PBMC的IL-1β释放。通过吸引更多的免疫细胞，并诱导免疫细胞释放促炎性IL-1β，CCL20可以延长溃疡性结肠炎的炎症反应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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