For example, IL-4−/− mice are more susceptible to lung injury following Streptococcus pneumoniae/influenza coinfection due to increases in both gasdermin D–induced pyroptosis of macrophages and higher concentrations of inflammatory cytokines, neither of which were observed in wild-type mice with intact IL-4 production.75 Furthermore, administration of recombinant IL-4 to coinfected IL-4−/− mice reduced IL-6, TNF-α, and IL-1β levels and the degree of lung injury.75 Here, IL4 is linked to influenza.