This strain represents a model of Ifnar1 knockout (KO), constructed by the deletion of exon 2 (E2) of the mouse Ifnar1 gene. This modification leads to a deficiency in the function of type I IFN receptors, resulting in a diminished immune response, heightened susceptibility to viral infections, and a decreased immune response to immunostimulatory DNA. Homozygous Ifnar1 KO mice are viable and fertile.