Irf7 Conditional Knockout mouse models

Serving as the master amplifier of the type I interferon system, Irf7 is the mouse ortholog of human IRF7 and encodes an interferon inducible regulatory factor that closes the positive feedback loop converting the single Ifnb1 first wave into broad interferon alpha subtype expression. In plasmacytoid dendritic cells it is activated MyD88 dependently through IRAK4, IRAK1, and IKKalpha downstream of endosomal TLR7 and TLR9, and in other cells by TBK1, with phosphorylation of the C-terminal serine cluster licensing dimerization and ISRE occupancy. Human IRF7 deficiency causes life threatening influenza with preserved responses to many other pathogens, while elevated interferon tone is central to lupus biology. Because Irf3 initiates and Irf7 amplifies, a single null blunts kinetics rather than abolishing induction, so compound alleles are frequently required. Conditional deletion with plasmacytoid dendritic cell restricted or Itgax-Cre drivers assigns the amplification compartment, and reporter knockins time the feedback loop without perturbing it.

Conditional deletion of Irf7 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Irf7 floxed stock yields usable cohorts.