...
首页> 外文期刊>Cellular immunology >IL-1B enhances human placenta-derived mesenchymal stromal cells ability to mediate Th1/Th2 and Th1/CD4(+)IL-10(+) T cell balance and regulates its adhesion, proliferation and migration via PD-L1
【24h】

IL-1B enhances human placenta-derived mesenchymal stromal cells ability to mediate Th1/Th2 and Th1/CD4(+)IL-10(+) T cell balance and regulates its adhesion, proliferation and migration via PD-L1

机译:IL-1B增强人胎盘衍生的间充质基质细胞,其能够介导TH / TH2和TH1 / CD4(+)IL-10(+)T细胞平衡并通过PD-L1调节其粘附性,增殖和迁移

获取原文
获取原文并翻译 | 示例
           

摘要

Human placenta-derived mesenchymal stromal cells (hPMSCs) are promising candidates for the treatment of graft-versus-host disease (GVHD), which is associated with high IL-1 beta levels. In this study, the effects of IL-1 beta and hPMSCs on each other were investigated by analyzing the proportion of Th1, Th2 and CD4(+)IL-10(+) T cells and PD-L1 expression, as well as the adhesion, migration, and proliferation of hPMSCs. The results showed that hPMSCs decreased IL-1 beta levels and downregulated Th1/Th2 and Th1/CD4(+)IL-10(+) T cells ratios in the GVHD model. The in vitro results revealed that IL-1 beta strengthened the hPMSCs capacity to reduce the Th1/Th2 and Th1/CD4(+)IL-10(+) T cell ratios, inhibited the adhesion and proliferation of hPMSCs and increased PD-L1 expression on hPMSCs via the JAK and NF-kappa B pathways. Overall, these findings suggested that hPMSCs alleviate GVHD by decreasing IL-1 beta level and maintaining the balance among different T cell subsets. IL-1 beta enhanced the ability of hPMSCs to balance different T cell subsets and inhibited hPMSCs adhesion and proliferation by regulating PD-L1 expression via the JAK and NF-kappa B pathways.
机译:人胎盘衍生的间充质基质细胞(HPMSCs)是治疗移植物与宿主疾病(GVHD)的候选者,其与高IL-1β水平相关。在该研究中,通过分析TH1,TH2和CD4(+)IL-10(+)T细胞和PD-L1表达的比例以及粘附性,研究IL-1β和HPMSCs彼此的效果。以及粘附性HPMSC的迁移和扩散。结果表明,HPMSCs在GVHD模型中降低了IL-1β水平和下调的TH1 / TH2和TH1 / CD4(+)IL-10(+)T细胞比率。体外结果表明,IL-1β强化了降低TH1 / TH2和TH1 / CD4(+)IL-10(+)T细胞比率的HPMSCS能力,抑制HPMSCs的粘附和增殖和增加的PD-L1表达通过JAK和NF-Kappa B途径在HPMSC上。总体而言,这些发现表明HPMSCS通过降低IL-1β水平并维持不同T细胞亚集之间的平衡来缓解GVHD。 IL-1β通过通过JAK和NF-Kappa B途径调节PD-L1表达,增强了HPMSCs平衡不同T细胞亚群的能力并抑制HPMSCs粘附和增殖。

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