Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus
Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus
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DOI：
10.1038/ni.2131
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发表时间：
2011-11-01
影响因子：
30.5
通讯作者：
Artis, David
中科院分区：
文献类型：
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作者：
Monticelli, Laurel A.;Sonnenberg, Gregory F.;Artis, David
先天性淋巴样细胞（ILC）是一种异质性细胞群，在协调肠道免疫和炎症中至关重要，但ILC是否影响其他粘膜部位的免疫反应或组织稳态仍然缺乏表征。在这里，我们确定了一个群体的肺居民ILCs在小鼠和人类表达同种异体抗原Thy-1（CD 90），白细胞介素2（IL-2）受体α链（CD 25），IL-7受体α链（CD 127）和IL-33受体亚基T1-ST 2。值得注意的是，小鼠ILC在感染流感病毒后在肺中积累，并且ILC的消耗导致气道上皮完整性丧失、肺功能减弱和气道重塑受损。这些缺陷通过给予肺ILC产物双调蛋白而恢复。总的来说，我们的研究结果表明，在流感病毒感染后，肺ILC在恢复气道上皮完整性和组织稳态方面发挥着关键作用。
Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor alpha-chain (CD25), IL-7 receptor alpha-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.