Ifnar2, also known as interferon alpha and beta receptor subunit 2, is a crucial component of the type I interferon receptor (IFNAR), which is formed along with Ifnar1. Type I interferons interact with IFNAR to amplify and propagate the antiviral response, playing central roles in regulating immune responses [1,2,4]. The receptor is involved in various biological processes such as antiviral immunity, anti-proliferative, anti-angiogenic, and immunomodulatory activities [1]. Genetic models, like knockout mice, have been valuable in studying its function.

In Ifnar2 knockout mice, the role of Ifnar2 in anti-influenza immunity was clearly demonstrated. Ifnar2 -/- mice displayed increased and accelerated morbidity and mortality compared to wild-type mice during influenza A virus (IAV) infection, indicating its critical role in antiviral immunity. Moreover, unlike Ifnar1 -/- mice, Ifnar2 -/- mice were not susceptible to bacterial superinfections (BSI) induced on day 3 post-IAV, despite increased viral burden and an inflammatory environment. However, similar to Ifnar1 -/- mice, they were less susceptible than wild-type mice to BSI induced on day 7 post-IAV [5]. In a mouse model of type 1 diabetes (T1D), knockdown of Ifnar2 reduced the inflammatory response and improved islet function, as IFNAR2 protein and mRNA expression were significantly higher in T1D mice compared to controls, and knockdown reversed the trends in various markers related to inflammation and islet function [3].

In conclusion, Ifnar2 is essential for antiviral immunity, as shown by knockout mouse models in influenza infection. It also plays a role in regulating the inflammatory response in diseases like type 1 diabetes. These model-based studies have provided insights into the functions of Ifnar2 in specific disease conditions, highlighting its significance in immune-related biological processes.