TGFB1 and influenza: Influenza A virus (IAV) drives enzymatic and integrin-mediated release of bioactive TGF-β1 into the airway lumen,44,46,49–51 including cleavage of latent TGF-β1 by the IAV neuraminidase,51 as well as de novo synthesis from club cells.44 Antibody blockade of all TGF-β isoforms during primary influenza infection enhances morbidity and mortality from 6 days post inoculation, suggesting that TGF-β is required to control the cell-mediated adaptive immune response, which peaks around this timepoint49 (Fig. 2b).