IL27 and influenza: In contrast to the inflammatory cytokines IL-12 or IL-23, which are rapidly produced by myeloid cells, e.g. upon triggering TLR receptors, and accordingly found in early time points in the influenza infection, the expression of IL-27 is turned on in a delayed fashion by the inflammatory microenvironment and serves as a negative feedback mechanism, thereby dampening the immune response in the later phase when adaptive immunity is established and the risk of severe immunopathology comes to the fore.