IFN-α is secreted by various cell types, triggering antiviral responses by stimulating macrophages and NK cells, and it also possesses anti-tumor activity. By altering the activity of heat-sensitive neurons in the hypothalamus, IFN-α acts as a pyrogen, causing fever. Similarly, IFN-α can alleviate pain by interacting with μ-opioid receptors, acting as an analgesic.All type I interferons (IFNs: IFN-α, IFN-β, IFN-ε, IFN-κ, and IFN-ω) bind to a common receptor on the surface of human cells, known as the type I IFN receptor. The type I IFN receptor consists of two subunits, IFNAR1 and IFNAR2, which associate with Janus-activated kinases (JAKs) TYK2 and JAK1, respectively. Activation of JAKs associated with the type I IFN receptor leads to phosphorylation of STAT2 and STAT1, resulting in the formation of the STAT1-STAT2-IRF9 complex, known as ISGF3 (interferon-stimulated gene factor 3) complex. These complexes translocate to the nucleus and bind to IFN-stimulated response elements in DNA to initiate gene transcription.IFNα Reporter THP1 Cell Line is a reporter gene cell line constructed based on the STATs signaling pathway. When IFN-α binds to the type I IFN receptor (IFNAR1 and IFNAR2), the signaling pathway is activated, forming the ISGF3 complex. The complex translocates to the nucleus and binds to IFN-stimulated response elements in DNA, thereby activating luciferase expression. Luciferase readings represent the activation effect of the signaling pathway and can be used for the in vitro evaluation of IFNα-related drug effects.
