...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Allergy >Serine protease allergen favours Th2 responses via PAR PAR ‐2 and STAT STAT 3 activation in murine model
【24h】

Serine protease allergen favours Th2 responses via PAR PAR ‐2 and STAT STAT 3 activation in murine model

机译：丝氨酸蛋白酶过敏原于通过PAR-2和STAT STAT 3激活鼠模型的响应

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

Abstract Background Protease activity of Per a 10 favours Th2 responses by differential regulation of IL ‐12p70 and IL ‐23 cytokine subunits. This study aimed to elucidate the underlying mechanism of differential regulation of IL ‐12p70 and IL ‐23. Methods PAR ‐2 activation was blocked in murine model by administering SAM 11 before each sensitization. CD 11c + p‐ STAT 3 + cells were measured in lungs by flow cytometry. BMDC s were pretreated with SAM 11 or isotype control or stattic and stimulated with Per a 10. p‐ STAT 3 levels were measured using Western blot. Transcript levels of IL ‐12p35, IL ‐12/23p40 and IL ‐23p19 were measured using RT ‐ PCR . Cytokine levels were analysed using ELISA . Results Protease activity of Per a 10 increased p‐ STAT 3 levels in mouse lungs, which was reduced upon PAR ‐2 blockage. Percentage of p‐ STAT 3 + CD 11c + cells was higher in Per a 10‐administered mice and was reduced upon PAR ‐2 blockage. IL ‐12p35 and IL ‐12p70 levels were higher, and IL ‐23p19 and IL ‐23 levels were lower in both SAM 11‐treated mice and BMDC s indicating a role of PAR ‐2‐mediated signalling. IL ‐4, TSLP , IL ‐17A, EPO activity, total cell count and specific IgE and IgG1 levels were lower in SAM 11‐administered mice. Inhibiting STAT 3 activation via stattic also leads to lower levels of IL ‐23p19 and IL ‐23 and higher levels of IL ‐12p35. Conclusions Per a 10 leads to PAR ‐2 activation on BMDC s resulting in downstream activation of STAT 3 to regulate the balance between IL ‐12/ IL ‐23 subunits causing a cytokine milieu rich in IL ‐23 to favour Th2 polarization.
机译：摘要通过IL -12P70和IL -23细胞因子亚基的差异调节，每10个抗差异调节的摘要背景蛋白酶活性。本研究旨在阐明IL -12P70和IL -23差异调节的潜在机制。方法通过在每次致敏之前通过施用SAM 11，在鼠模型中封闭PAR-2激活。通过流式细胞术测量CD 11C + P-STAT 3 +细胞。 BMDC S用SAM 11或同种型对照或STATTIC进行预处理，并用每10次刺激。使用Western印迹测量P-Stat 3水平。使用RT - PCR测量IL -12P35，IL -12 / 23P40和IL -23P19的转录物水平。使用ELISA分析细胞因子水平。结果每次10％的蛋白酶活性增加小鼠肺部的P-Stat 3水平，在PAR-2堵塞时降低。 P-STAT 3 + CD 11C +细胞的百分比每种施用的小鼠较高，并在PAR -2封闭时减少。 IL -12P35和IL -12P70水平较高，SAM 11处理的小鼠和BMDC S中的IL -23P19和IL -23水平较低，表明PAR-2介导的信号传导的作用。在SAM 11给药的小鼠中，IL-4，TSLP，IL -17A，EPO活性，总细胞计数和特定IgE和IgG1水平较低。抑制STAT 3通过STATTIC激活也导致IL -23P19和IL -23的较低水平和更高水平的IL -12P35。结论每10例导致BMDC S的pAR-2激活导致STAT 3下游激活，以调节IL -12 / IL -23亚基之间的平衡，导致富含IL -23的细胞因子Milieu，以支持Th2极化。

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