...
首页> 外文期刊>Cytokine >The effect of adenosine receptor agonists on cytokine release by human mononuclear cells depends on the specific Toll-like receptor subtype used for stimulation.
【24h】

The effect of adenosine receptor agonists on cytokine release by human mononuclear cells depends on the specific Toll-like receptor subtype used for stimulation.

机译:腺苷受体激动剂对人单核细胞释放细胞因子的影响取决于用于刺激的特定Toll样受体亚型。

获取原文
获取原文并翻译 | 示例
           

摘要

In the present study, we determined whether the immunomodulatory effect of adenosine receptor stimulation depends on the Toll-like Receptor (TLR) used for stimulation of cytokine release. Therefore, human mononuclear cells were stimulated by different TLR agonists in the absence and presence of A1 (CPA), A2a (CGS21680), and A3 (Cl-IB-MECA) adenosine receptor agonists. Effects of these agonists on Il-6, Il-10, IFN-gamma, TNF-alpha, and Il-1beta production were expressed as percentage inhibition/stimulation after TLR stimulation. CGS21680 inhibited TLR4-mediated TNF-alpha release and potentiated TLR3- and TLR5-mediated IL-6 release. Cl-IB-MECA inhibited TLR4-agonist-induced IFN-gamma release. Interestingly, CPA en Cl-IB-MECA tended to inhibit cytokine release only after TLR4 stimulation. In more detail, CPA potentiated TLR5-mediated IL-6 production, TLR3-mediated IFN-gamma production and TLR3-mediated Il-1beta-production compared to TLR4-mediated stimulation. Cl-IB-MECA potentiated TLR5-mediated IL-6 andIl-1beta formation as compared to TLR4-mediated stimulation. Finally, CGS21680 potentiated TLR5-mediated IL-6 production compared to TLR1-2 stimulation, and potentiated TLR3- and TLR5-mediated IL-10 production compared to TLR1-2-mediated stimulation. In conclusion, the effect of adenosine agonists on cytokine production depends on the specific TLR agonist used for stimulation. These findings suggest that well-known anti-inflammatory effects of adenosine agonists on LPS-induced inflammation cannot be extrapolated to situations in which stimulation of other TLR subtypes is involved.
机译:在本研究中,我们确定了腺苷受体刺激的免疫调节作用是否取决于刺激细胞因子释放的Toll样受体(TLR)。因此,在不存在和存在A1(CPA),A2a(CGS21680)和A3(C1-IB-MECA)腺苷受体激动剂的情况下,人类单核细胞会受到不同的TLR激动剂的刺激。这些激动剂对II-6,II-10,IFN-γ,TNF-α和II-1β产生的影响表示为TLR刺激后的抑制/刺激百分比。 CGS21680抑制TLR4介导的TNF-α释放,并增强TLR3和TLR5介导的IL-6释放。 Cl-IB-MECA抑制TLR4-激动剂诱导的IFN-γ释放。有趣的是,CPA en Cl-IB-MECA仅在TLR4刺激后才倾向于抑制细胞因子的释放。更详细地,与TLR4介导的刺激相比,CPA增强了TLR5介导的IL-6产生,TLR3介导的IFN-γ产生和TLR3介导的Il-1beta产生。与TLR4介导的刺激相比,C1-IB-MECA增强了TLR5介导的IL-6和II-1β的形成。最后,与TLR1-2刺激相比,CGS21680增强了TLR5介导的IL-6产生,而与TLR1-2刺激相比则增强了TLR3和TLR5介导的IL-10产生。总之,腺苷激动剂对细胞因子产生的影响取决于用于刺激的特异性TLR激动剂。这些发现表明,腺苷激动剂对LPS诱导的炎症的众所周知的抗炎作用不能推断为涉及其他TLR亚型刺激的情况。

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