Ifnar1, the Interferon Alpha Receptor 1, is a crucial subunit of the type I interferon receptor (IFNAR). Type I interferon signaling, in which Ifnar1 is involved, plays a vital role in the restriction or eradication of pathogen invasion, innate and adaptive antiviral immunity, and is associated with various biological processes [1,4]. Genetic models, such as knockout (KO) mouse models, are valuable tools for studying its functions.

In Ifnar1 -deficient mice, several significant findings have been reported. In the context of virus infection, genetic ablation of Ifnar1 specifically in natural killer (NK) cells led to improved antiviral T cell function and hastened virus clearance, suggesting that Ifnar1 signaling in NK cells promotes persistent virus infection [2]. In tumor-related studies, Ifnar1 -/- mice showed elevated tumor growth, as inactive Ifnar1 led to impaired immunostimulatory properties of neutrophils in tumor-draining lymph nodes, reducing their ability to interact with and stimulate T-cells [3]. Also, SFTS virus infection in Ifnar1 -/- mice caused activation of neurotoxic A1-reactive astrocytes, accelerating fatal brain damage [5]. Moreover, construction of an Ifnar1 knockout MDBK cell line increased the titers of bovine viruses, revealing its role in restricting viral replication in bovine cells [6].

In conclusion, Ifnar1 is essential for the body's antiviral defense and immune-related functions. Studies using Ifnar1 KO mouse models have provided valuable insights into its role in viral infections, tumor growth, and neuroinflammatory diseases, enhancing our understanding of the underlying biological mechanisms and potentially guiding the development of new therapeutic strategies in these disease areas.