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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Negative regulation of eosinophil recruitment to the lung by the chemokine monokine induced by IFN-γ (Mig, CXCL9)
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Negative regulation of eosinophil recruitment to the lung by the chemokine monokine induced by IFN-γ (Mig, CXCL9)

机译：IFN-γ诱导的趋化因子单因子对嗜酸性粒细胞向肺募集的负调控（Mig，CXCL9）

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摘要

Experimental analysis of allergic airway inflammation (AAI) in animals and humans is associated with coordinate gene induction. Using DNA microarray analysis, we have identified a large panel of AAI signature genes. Unexpectedly, the allergen-challenged lung (a T helper 2 microenvironment) was found to be associated with the expression of T helper 1-associated CXCR3 ligands, monokine induced by IFN-γ (Mig), and IFN-γ-inducible protein of 10 kDa (IP-10). Here we report that Mig functions as a negative regulator of murine eosino-phils. Whereas Mig was not able to induce chemotaxis of eosinophils, pretreatment with Mig induced a dose-dependent inhibition of che-moattractant-induced eosinophil transmigration in vitro. Moreover, i.v. administration of low doses of Mig (≈10-30 μg/kg) induced strong and specific dose-dependent inhibition of chemokine-, IL-13-, and allergen-induced eosinophil recruitment and, conversely, neutralization of Mig before allergen challenge increased airway eosin-ophilia. Importantly, Mig also inhibited a CCR3-mediated functional response in eosinophils. These results indicate that the ultimate distribution and function of inflammatory cells within the allergic lung is dictated by a balance between positively and negatively regulatory chemokines. The identification of a naturally occurring eosinophil inhibitory chemokine pathway in vivo provides a strategic basis for future therapeutic consideration.
机译：动物和人类中过敏性气道炎症（AAI）的实验分析与协调基因诱导相关。使用DNA芯片分析，我们确定了一大批AAI签名基因。出乎意料的是，发现变应原激发的肺（T辅助2微环境）与T辅助1相关的CXCR3配体的表达，IFN-γ（Mig）诱导的单因子和IFN-γ诱导的10蛋白表达有关kDa（IP-10）。在这里，我们报告说Mig充当小鼠嗜酸性粒细胞的负调节剂。 Mig不能诱导嗜酸性粒细胞趋化性，而Mig预处理则在体外诱导剂量依赖性抑制化学引诱剂诱导的嗜酸性粒细胞迁移。此外，i.v。给予低剂量的Mig（≈10-30μg/ kg）会强烈且特异性地抑制趋化因子，IL-13和变应原诱导的嗜酸性粒细胞募集，并且相反，在变应原激发之前，Mig的中和作用会增加气道嗜酸性粒细胞增多。重要的是，Mig还抑制了嗜酸性粒细胞中CCR3介导的功能反应。这些结果表明，过敏性肺内炎性细胞的最终分布和功能由正向和负向调节趋化因子之间的平衡决定。体内天然存在的嗜酸性粒细胞抑制趋化因子途径的鉴定为将来的治疗考虑提供了战略基础。

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