In mice infected with a sub-lethal dose of H3N2 Influenza A, ILCs had enhanced expression of IL-22 transcripts as early as 2 days post-infection, and mice able to produce IL-22 had reduced lung injury and better protection from post-influenza Streptococcus pneumoniae superinfection, in comparison to IL-22-deficient animals (28). This evidence concerns the gene IL22 and infection.