Mouse Interferon Gamma Receptor 1 (IFNGR1) Protein

Background

Interferon Gamma Receptor 1 (IFNGR1) is a pivotal transmembrane protein that serves as the primary receptor for interferon-gamma (IFN-γ), a crucial cytokine involved in innate and adaptive immune responses. IFNGR1 is predominantly expressed on the surface of immune cells, such as macrophages, T lymphocytes, and natural killer (NK) cells, and also on various non-immune cell types. Structurally, IFNGR1 is composed of an extracellular domain that binds IFN-γ, a transmembrane region, and a cytoplasmic tail that interacts with downstream signaling components. Upon IFN-γ binding, IFNGR1 forms a functional receptor complex with IFNGR2, initiating the JAK-STAT signaling cascade. This pathway leads to the activation of STAT1, which translocates to the nucleus to regulate the transcription of genes involved in antimicrobial defense, antigen presentation, and immune cell differentiation. Genetic mutations or deficiencies in IFNGR1 can result in immunodeficiencies, such as Mendelian susceptibility to mycobacterial diseases (MSMD), characterized by impaired responses to intracellular pathogens like mycobacteria and certain viruses. Due to its central role in immune regulation, IFNGR1 is extensively studied in the context of infectious diseases, autoimmunity, and cancer immunotherapy, where modulating its activity could enhance immune responses or mitigate pathological inflammation.