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气道上皮细胞通过 IFNγ/STAT1/TGFβ 依赖的机制抑制 T 细胞增殖。

Airway epithelial cells suppress T cell proliferation by an IFNγ/STAT1/TGFβ-dependent mechanism.

机构信息

Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2012 Jan 1;302(1):L167-73. doi: 10.1152/ajplung.00188.2011. Epub 2011 Oct 14.

Abstract

Organ-specific regulation of immune responses relies on the exchange of information between nonimmune and immune cells. In a primary culture model of the lung airway, we demonstrate that T cell proliferation is potently inhibited by airway epithelial cells (ECs). This is mediated by activation of the IFNγ/STAT1 pathway in the EC and transforming growth factor-β (TGFβ)-dependent suppression of T cell proliferation. In this way, the EC can restrict the expansion of T cells. Given the constant exposure of the airway to inhaled antigen, this may be important in setting a threshold for the initiation of T cell-dependent immune responses and preventing unwanted, chronic inflammation.

摘要

器官特异性免疫反应的调节依赖于非免疫细胞和免疫细胞之间的信息交换。在肺气道的原代细胞培养模型中,我们证明气道上皮细胞(EC)可强烈抑制 T 细胞增殖。这是通过 EC 中 IFNγ/STAT1 途径的激活以及 TGFβ依赖性抑制 T 细胞增殖来介导的。通过这种方式,EC 可以限制 T 细胞的扩增。考虑到气道持续暴露于吸入抗原,这对于设定 T 细胞依赖性免疫反应的启动阈值和防止不必要的慢性炎症可能很重要。

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