Pulmonary IL-27 levels peaked late in influenza infection, and delivery of recombinant IL-27 at this stage of infection limited recruitment of inflammatory monocytes, neutrophils, and NK cells into the lung, without affecting the T cell response, suggesting that IL-27 can operate at multiple levels to control the immune response to influenza.140 Others have reported the role of IL-27, produced by lung APCs in a type 1 IFN-dependent manner,141 in generation of IL-10+ CD8+ T cells,142 a key regulatory population during influenza infection94 (see above). This evidence concerns the gene IL10 and infection.