| First Author | Chang YJ | Year | 2011 |
| Journal | Nat Immunol | Volume | 12 |
| Issue | 7 | Pages | 631-8 |
| PubMed ID | 21623379 | Mgi Jnum | J:174316 |
| Mgi Id | MGI:5056254 | Doi | 10.1038/ni.2045 |
| Citation | Chang YJ, et al. (2011) Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity. Nat Immunol 12(7):631-8 |
| abstractText | 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. |
