首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Mesenchymal stem cells promote CD206 expression and phagocytic activity of macrophages through IL-6 in systemic lupus erythematosus
【24h】

Mesenchymal stem cells promote CD206 expression and phagocytic activity of macrophages through IL-6 in systemic lupus erythematosus

机译:间质干细胞通过系统性红斑狼疮中的IL-6促进巨噬细胞的CD206表达和吞噬活性

获取原文
获取原文并翻译 | 示例
           

摘要

Human umbilical cord-derived mesenchymal stem cells (UCMSCs) show therapeutic effects on systemic lupus erythematosus (SLE). Deficiency in functional polarization and phagocytosis in macrophages has been suggested in the pathogenesis of SLE. We found that macrophages from B6.MRL-Fas(lpr) mice exhibited lower level of CD206, the marker for alternatively activated macrophage (AAM, also called M2). In addition, the phagocytic activity of B6.MRL-Fas(lpr) macrophages was also decreased. UCMSC transplantation improved the proportion of CD206(+) macrophages and their phagocytic activity in B6.MRL-Fas(lpr) mice. Importantly, macrophages from SLE patients also showed lower expression of CD206 and reduced phagocytic activity, which were corrected by being co-cultured with UCMSCs in vitro and in SLE patients receiving UCMSC transplantation. Mechanistically, we demonstrated that IL-6 was required for the up-regulation of CD206 expression and phagocytic activity of UCMSC-treated SLE macrophages. Our results indicate that UCMSCs alleviate SLE through promoting CD206 expression and phagocytic activity of macrophages in an IL-6 dependent manner. (C) 2015 Elsevier Inc. All rights reserved.
机译:人脐带间充质干细胞(UCMSCs)对系统性红斑狼疮(SLE)有治疗作用。在SLE的发病机理中已经提出巨噬细胞功能极化和吞噬作用的缺乏。我们发现,来自B6.MRL-Fas(lpr)小鼠的巨噬细胞表现出较低水平的CD206,CD206是交替激活的巨噬细胞(AAM,也称为M2)的标记。此外,B6.MRL-Fas(lpr)巨噬细胞的吞噬活性也降低了。 UCMSC移植改善了B6.MRL-Fas(lpr)小鼠中CD206(+)巨噬细胞的比例及其吞噬活性。重要的是,SLE患者的巨噬细胞还显示出CD206的表达降低和吞噬活性降低,这可以通过与UCMSCs体外共培养以及接受UCMSC移植的SLE患者进行纠正。从机制上讲,我们证明IL-6是UCMSC处理的SLE巨噬细胞CD206表达和吞噬活性上调所必需的。我们的结果表明,UCMSC通过以IL-6依赖性方式促进CD206表达和巨噬细胞的吞噬活性来减轻SLE。 (C)2015 Elsevier Inc.保留所有权利。

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