Our findings define roles for myeloid TBK1 in IAV-induced lung inflammation apart from IFN type I expression and point to myeloid TBK1 as a central and cell type-specific regulator of virus-induced lung damage.
<i>In vivo</i>, ExoT also increases IFN-γ levels and the percentage of IFN-γ<sup>+</sup> NK cells in lungs during PA pneumonia, confirming <i>in vitro</i> data.