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IL-2 控制着 trafficking receptor 基因的表达和 Th2 反应,从而引发皮肤和肺部炎症。

IL-2 controls trafficking receptor gene expression and Th2 response for skin and lung inflammation.

机构信息

Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, VA 22908-0133, USA.

出版信息

Clin Immunol. 2012 Oct;145(1):82-8. doi: 10.1016/j.clim.2012.07.015. Epub 2012 Aug 4.

Abstract

Both Il2(-/-) mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2(-/-) double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its "organ-specific" pro-inflammatory function by regulating the migration and retention of CD4(+) T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2-regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung.

摘要

IL2(-/-) 小鼠和 Scurfy (Sf) 突变小鼠缺乏 FoxP3,都会发展为多器官炎症,但只有后者表现出严重的皮肤和肺部炎症。相比之下, Sf.Il2(-/-) 双突变小鼠不会出现皮肤炎症,肺部炎症也明显减轻。在这篇综述中,我们总结了我们最近的研究结果,这些结果基于对 10 只 Sf 双突变小鼠的微阵列、q-PCR 和功能研究。这些研究揭示了 IL-2 在以器官特异性方式调节炎症方面的新的促炎功能。IL-2 通过调节 CD4(+)T 细胞(Th1 和 Th2 细胞)向皮肤和肺部的迁移和保留来发挥其“器官特异性”促炎作用。此外,IL-2 还需要调节 T 细胞激活过程中的 Th2 细胞因子反应。对这些受 IL-2 调节的基因的进一步研究将有助于确定干预皮肤和肺部炎症性疾病的新靶点。

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