...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Intravascular inactivation of CCR5 by n-Nonanoyl-CC chemokine ligand 14 and inhibition of allergic airway inflammation.
【24h】

Intravascular inactivation of CCR5 by n-Nonanoyl-CC chemokine ligand 14 and inhibition of allergic airway inflammation.

机译：n-壬酰基-CC趋化因子配体14对CCR5的血管内灭活作用和对过敏性气道炎症的抑制作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Modulation of leukocyte recruitment through intervention with chemokine receptors is an attractive, therapeutic strategy. Recently, we have shown that n-Nonanoyl (NNY)-CCL14 internalizes and desensitizes human (h)CCR3, resulting in the inactivation of eosinophils. In this study, we investigated the interaction of NNY-CCL14 with CCR1 and CCR5 and the relevance of these NNY-CCL14 receptors on its in vivo effects in allergic airway inflammation. NNY-CCL14 has inactivating properties on CCR1(+) and CCR5(+) cell lines and primary leukocytes. It desensitizes hCCR1- and hCCR5-mediated calcium release and internalizes these receptors from the cellular surface. Treatment of OVA-sensitized BALB/c mice with NNY-CCL14 resulted in reduced pulmonary inflammation. Above all, it is demonstrated that systemic treatment with NNY-CCL14 down-modulates CCR5 from the surface of lymphocytes in vivo. Although NNY-CCL14 acts on murine lymphocytes and internalizes CCR5, it does not internalize CCR3 on mouse eosinophils, showingspecies selectivity regarding this particular receptor. Therefore, the inhibitory effects of NNY-CCL14 in murine models of allergic airway inflammation can be assigned to its interaction with CCR5. The presented results substantiate the relevance of CCR5 as a target for allergic airway inflammation.
机译：通过趋化因子受体的干预来调节白细胞募集是一种有吸引力的治疗策略。最近，我们已经显示正壬酰基（NNY）-CCL14使人（h）CCR3内化和脱敏，导致嗜酸性粒细胞失活。在这项研究中，我们调查了NNY-CCL14与CCR1和CCR5的相互作用，以及这些NNY-CCL14受体对其在变应性气道炎症中的体内作用的相关性。 NNY-CCL14在CCR1（+）和CCR5（+）细胞系和原代白细胞上具有失活特性。它使hCCR1和hCCR5介导的钙释放脱敏，并使这些受体从细胞表面内化。用NNY-CCL14治疗OVA致敏的BALB / c小鼠可减少肺部炎症。最重要的是，证明了用NNY-CCL14进行的全身治疗在体内从淋巴细胞表面下调了CCR5。尽管NNY-CCL14作用于鼠淋巴细胞并内化CCR5，但它并未内化小鼠嗜酸性粒细胞上的CCR3，显示出对该特定受体的选择性。因此，NNY-CCL14在变应性气道炎症的鼠模型中的抑制作用可归因于其与CCR5的相互作用。提出的结果证实了CCR5作为过敏性气道炎症的靶标的相关性。

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