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目的 研究γIP 1 0和Mig通过趋化因子CXC受体 3 (CXCR3 )激活嗜酸性粒细胞的活化细胞核因子 (nuclearfactorofactivatedTlymphocytes,NFAT)作用。方法 嗜酸性粒细胞的纯化技术、流式细胞术、实时定量逆转录PCR (RT PCR)、核提取物和电泳移动性转变测定等方法进行测定与分析。结果 CXCR3大量在嗜酸性粒细胞上表达。通过流式细胞仪及实时定量RT PCR技术检测证明 ,IL 2和IL 1 0上调或下调嗜酸性粒细胞上CXCR3的蛋白和mRNA表达水平。其配体γIP 1 0和Mig可以引起嗜酸性粒细胞中的NFAT复合体的核易位而激活NFAT1和NFAT4。结论 CXCR3 γIP 1 0和 Mig受体 配体以及IL 2和IL 1 0对CXCR3表达的调节作用可能在过敏炎症过程 (包括启动、发展和结局的病理生理过程 )的细胞因子 /趋化因子环境中发挥特别重要的作用。
Objective To investigate the role of γIP 1 0 and Mig in activation of eosinophils activated nuclear factor (NFAT) by chemokine CXC receptor 3 (CXCR3). Methods Eosinophil purification, flow cytometry, real-time quantitative reverse transcription PCR (RT PCR), nuclear extract and electrophoretic mobility shift assay and other methods were measured and analyzed. As a result CXCR3 was abundantly expressed on eosinophils. The results of flow cytometry and real-time RT-PCR showed that IL-2 and IL-10 upregulated or down-regulated the protein and mRNA expression of CXCR3 on eosinophils. Its ligands [gamma] IP10 and Mig can activate NFATl and NFAT4 by causing nuclear translocation of the NFAT complex in eosinophils. Conclusions The regulatory effect of CXCR3 γIP 10 and Mig receptor ligands and IL 2 and IL 10 on CXCR3 expression may be in the cytokine / chemokine environment of allergic inflammatory processes, including the pathophysiological processes of priming, development and outcome Play a particularly important role.