Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity.
摘要：
Patients with asthma, a major public health problem, are at high risk for serious disease from influenza virus infection, but the pathogenic mechanisms by which influenza A causes airway disease and asthma are not fully known. We show here in a mouse model that influenza infection acutely induced airway hyper-reactivity (AHR), a cardinal feature of asthma, independently of T helper type 2 (T(H)2) cells and adaptive immunity. Instead, influenza infection induced AHR through a previously unknown pathway that required the interleukin 13 (IL-13)-IL-33 axis and cells of the non-T cell, non-B cell innate lymphoid type called 'natural helper cells'. Infection with influenza A virus, which activates the NLRP3 inflammasome, resulted in much more production of IL-33 by alveolar macrophages, which in turn activated natural helper cells producing substantial IL-13.
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关键词：
Animals Mice, Inbred BALB C Mice T-Lymphocytes, Helper-Inducer Macrophages, Alveolar Influenza A virus Orthomyxoviridae Infections Asthma Bronchial Hyperreactivity Interleukins
DOI：
10.1038/ni.2045
被引量：
年份：
2011
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