| First Author | Kumagai Y | Year | 2007 |
| Journal | Immunity | Volume | 27 |
| Issue | 2 | Pages | 240-52 |
| PubMed ID | 17723216 | Mgi Jnum | J:124340 |
| Mgi Id | MGI:3721349 | Doi | 10.1016/j.immuni.2007.07.013 |
| Citation | Kumagai Y, et al. (2007) Alveolar Macrophages Are the Primary Interferon-alpha Producer in Pulmonary Infection with RNA Viruses. Immunity 27(2):240-52 |
| abstractText | Type I interferons (IFNs) are critical for antiviral responses. Here we generated a knockin mouse in which green fluorescence protein (GFP) was expressed under the control of the Ifna6 promoter. Virus-induced expression of GFP recapitulated various IFN-alpha subtypes. Systemic infection of the mice with Newcastle disease virus (NDV) increased GFP(+) plasmacytoid dendritic cells (pDCs) via the Toll-like receptor system, and GFP(+) conventional dendritic cells (cDCs) and macrophages via the RIG-I-like helicase system. By contrast, lung infection with NDV led to IFN-alpha production in alveolar macrophages (AMs) and cDCs, but not in pDCs. Specific depletion of AMs caused a marked defect in the initial viral elimination in the lung. pDCs produced IFN-alpha in the absence of AM-mediated viral recognition, suggesting that pDCs function when the first defense line is broken. Thus, AMs act as a type I IFN producer that is important for the initial responses to viral infection in the lung. |
