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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >STAT4/6-dependent differential regulation of chemokine receptors.
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STAT4/6-dependent differential regulation of chemokine receptors.

机译：STAT4 / 6依赖性趋化因子受体的差异调节。

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摘要

The major cell fate decision of the CD4+ helper T cells is the development of Th1 and Th2 phenotype, the balance of which determines the outcome of a wide variety of autoimmune responses. Signal transducers and activators of transcription (STATs), in particular STAT4 and STAT6, are essential for the development of Th1 and Th2 cells, respectively. We used Balb/c mice lacking STAT4 or STAT6 to explore the ability of helper T cells to express chemokine receptors. We demonstrated that both STAT4-/- and STAT6-/- CD4+ lymphocytes showed impaired expansion as well as differentiation into IFN-gamma-secreting Th1 cells and IL2-, IL4-, IL10-secreting Th2 cells. Interestingly, the expression of chemokine receptors, which is STAT4/6-dependent, was differentially regulated via two distinct mechanisms, positively (CCR3, CCR4) and negatively (CCR5, CCR7). These results provide the basis for STAT-dependent differential regulation of chemokine receptors in Th subsets.
机译：CD4 +辅助T细胞的主要细胞命运决定是Th1和Th2表型的发展，其平衡决定了多种自身免疫反应的结果。信号转导子和转录激活子（STATs），尤其是STAT4和STAT6，分别对于Th1和Th2细胞的发育至关重要。我们使用缺少STAT4或STAT6的Balb / c小鼠来探索辅助性T细胞表达趋化因子受体的能力。我们证明，STAT4-/-和STAT6-/-CD4 +淋巴细胞均显示出受损的扩张以及分化为分泌IFN-γ的Th1细胞和分泌IL2，IL4，IL10的Th2细胞的分化。有趣的是，依赖于STAT4 / 6的趋化因子受体的表达通过两种不同的机制（正向（CCR3，CCR4）和负向（CCR5，CCR7））被不同地调节。这些结果为Th亚群中趋化因子受体的STAT依赖性差异调节提供了基础。

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