IFNAR2

IFNAR2, or Interferon Alpha and Beta Receptor Subunit 2, is a crucial component of the type I interferon receptor complex, predominantly expressed on the surface of immune cells. It plays an essential role in mediating antiviral and antiproliferative responses by facilitating the binding and signal transduction of type I interferons, such as IFN-α and IFN-β. Through its interaction with these interferons, IFNAR2 activates downstream signaling pathways, including the JAK-STAT (Janus kinase-signal transducer and activator of transcription) pathway, leading to the expression of interferon-stimulated genes that enhance antiviral defenses and modulate immune responses. Dysregulation of IFNAR2, whether through mutations, overexpression, or altered timing of expression, can disrupt these pathways, resulting in impaired immune function or inappropriate immune activation, which has been implicated in conditions such as multiple sclerosis and systemic lupus erythematosus. Researchers and clinicians explore IFNAR2 function and its modulation through various methods, including the use of monoclonal antibodies and small-molecule inhibitors, to either block or enhance its signaling capacity. These interventions are pivotal in studying the protein's role in immune regulation and in developing therapeutic strategies for diseases with an immune component. For example, in viral infections, modulation of IFNAR2 activity can help delineate its contribution to host defense mechanisms, providing insights into potential treatment avenues. Additionally, measuring IFNAR2 levels or activity can serve as a biomarker for immune system status, offering clinicians a tool for diagnosing or monitoring diseases characterized by immune dysregulation.