IL-33 has been shown to be an important activator of ILC2s in mouse models of allergic airway inflammation, influenza infection, and rhinovirus infection.12, 14, 16, 18, 19, 21, 46, 47 Interestingly, we found similar numbers of IL-13–producing ILC2s after RSV infection in IL-33–deficient mice, although there was a statistically significant decrease in the total lung concentration of IL-13 at day 4 after infection. This evidence concerns the gene IL33 and infection.