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. 2016 Aug;37(4):487–500. doi: 10.1055/s-0036-1584801

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Fig. 2 — Key players in influenza A virus (IAV)-induced lung injury. While upper respiratory tract infection results in mild symptomatic IAV infection, severe cases of IAV usually involve spread of the virus to the lower respiratory tract. Here, resident alveolar macrophages (AM) and dendritic cells (DC) sense IAV infection of alveolar epithelial type I (AEC I) and type II (AEC II) cells. Cytokine release and establishment of a proinflammatory milieu in the alveolar lumen lead to recruitment of additional monocyte-derived macrophages (MDM) as well as neutrophils from the blood vessels to the site of infection. DC migration to the lymph nodes further induces generation of antigen-specific T cells into the vessel. An exuberant immune response with massive release of proinflammatory and proapoptotic mediators contributes to IAV-induced lung injury.