Schnurri-2 regulates Th2-dependent airway inflammation and airway hyperresponsiveness
Schnurri-2 regulates Th2-dependent airway inflammation and airway hyperresponsiveness
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DOI：
10.1093/intimm/dxm042
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发表时间：
2007-06-01
影响因子：
4.4
通讯作者：
Nakayama, Toshinori
中科院分区：
文献类型：
--
作者：
Iwamura, Chiaki;Kimura, Motoko Y.;Nakayama, Toshinori
Schnurri（Shn）-2是一种含锌指的蛋白质，在细胞生长、信号转导和淋巴细胞发育中起关键作用。在Shn-2缺陷型（Shn-2（-l-））CD 4 T细胞中，核因子-KB的活化被上调，并且它们分化成T（h）2的能力增强。在这里，我们扩展我们的调查，并证明Shn-2调节T（h）2反应在体内使用卵清蛋白诱导的过敏性哮喘模型。Shn-2（-/-）小鼠的嗜酸性粒细胞炎症、粘液分泌过多和气道高反应性（AHR）均增强。此外，在给予Shn-2（-/-）效应T（h）2转移的小鼠中，嗜酸性粒细胞浸润和AHR增强。因此，T（h）2中的Shn-2被认为在变应性气道炎症中作为负调节剂发挥重要作用。
Schnurri (Shn)-2 is a large zinc finger-containing protein, which plays a critical role in cell growth, signal transduction and lymphocyte development. In Shn-2-deficient (Shn-2(-l-)) CD4 T cells, the activation of nuclear factor-KB is up-regulated and their ability to differentiate into T(h)2 is enhanced. Here, we extend our investigation and demonstrate that Shn-2 regulates T(h)2 responses in vivo using an ovalbumin-induced allergic asthma model. Eosinophilic inflammation, mucus hyperproduction and airway hyperresponsiveness (AHR) were all enhanced in Shn-2(-/-) mice. Moreover, eosinophilic infiltration and AHR were enhanced in mice given a transfer of Shn-2(-/-) effector T(h)2. Shn-2 in T(h)2 is thus considered to play an important role as a negative regulator in allergic airway inflammation.