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IFN-γ increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells.

IFN-γ increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells.
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Califano D, Furuya Y, Roberts S, Avram D, McKenzie ANJ, Metzger DW,


Califano D, Furuya Y, Roberts S, Avram D, McKenzie ANJ, Metzger DW, (click to view)

Califano D, Furuya Y, Roberts S, Avram D, McKenzie ANJ, Metzger DW,

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Mucosal immunology 2017 05 1711(1) 209-219 doi 10.1038/mi.2017.41
Abstract

Increased levels of interferon-γ (IFN-γ) are routinely observed in the respiratory tract following influenza virus infection, yet its potential role remains unclear. We now demonstrate that influenza-induced IFN-γ restricts protective innate lymphoid cell group II (ILC2) function in the lung following challenge with the pandemic H1N1 A/CA/04/2009 (CA04) influenza virus. Specifically, IFN-γ deficiency resulted in enhanced ILC2 activity, characterized by increased production of interleukin (IL)-5 and amphiregulin, and improved tissue integrity, yet no change in ILC2 numbers, viral load or clearance. We further found that IFN-γ-deficient mice, as well as wild-type animals treated with neutralizing anti-IFN-γ antibody, exhibited decreased susceptibility to lethal infection with H1N1 CA04 influenza virus, and moreover that survival was dependent on the presence of IL-5. The beneficial effects of IFN-γ neutralization were not observed in ILC2-deficient animals. These data support the novel concept that IFN-γ can have a detrimental role in the pathogenesis of influenza through a restriction in ILC2 activity. Thus, regulation of ILC2 activity is a potential target for post-infection therapy of influenza.

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