Most influenza-related deaths are caused by influenza pneumonitis, a serious complication of influenza virus infection characterised by uncontrolled lung inflammation, acute lung injury and respiratory failure. This serious complication has a high mortality risk (18–32%) [1]. The currently available antiviral therapy (e.g. neuraminidase inhibitor) has limited efficacy in reducing fatality caused by influenza pneumonitis.

Host factors, in additional to viral factors, are important in determining patient outcomes in influenza pneumonitis [2, 3]. A better understanding of the host factors associated with severe disease is therefore needed; it may help discover pathogenic pathways that determine disease progression and enable researchers identify new therapeutic targets. Here, we examine the immune cells underpinning the host response to influenza infection.