The Ifnar1 gene encodes the interferon-alpha/beta receptor 1 subunit, a critical mediator of the body's antiviral and immune responses. This gene is predominantly expressed in immune cells, including lymphocytes and dendritic cells, and is also present in various tissues such as the liver, brain, and skin. The protein product of Ifnar1 forms a receptor complex with Ifnar2, which is essential for the binding of interferons alpha and beta. This ligand-receptor interaction initiates a cascade of signaling pathways, culminating in the activation of genes responsible for antiviral protein production, cell growth inhibition, and immune cell recruitment. The Ifnar1 gene plays a pivotal role in host defense, regulating a broad spectrum of processes including cellular growth, survival, differentiation, pathogen resistance, and antiviral immunity. Mutations or dysregulation of Ifnar1 can result in severe pathologies, such as systemic lupus erythematosus, characterized by excessive immune activation and tissue damage, or certain cancers, where compromised interferon signaling undermines anti-tumor immunity.

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.