IFN-α is secreted by various types of cells, triggering antiviral responses by stimulating macrophages and NK cells, and exhibiting antitumor activity. By altering the activity of thermosensitive neurons in the hypothalamus, IFN-α acts as a pyrogen, causing fever. Through a similar mechanism, IFN-α can be used to 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 called the Type I IFN receptor. The Type I IFN receptor is composed of two subunits, IFNAR1 and IFNAR2, which are associated with Janus-activated kinase (JAK) tyrosine kinase 2 (TYK2) and JAK1, respectively. Activation of JAKs associated with the Type I IFN receptor leads to tyrosine phosphorylation of STAT2 and STAT1; this results in the formation of the STAT1-STAT2-IRF9 complex, known as ISGF3 (interferon-stimulated gene factor 3) complex. These complexes translocate to the cell nucleus and bind to IFN-stimulated response elements in DNA to initiate gene transcription.IFNα Reporter HEK-293 Cell Line is a luciferase reporter cell line based on the STAT signaling pathway. When IFN-α binds to the Type I IFN receptor (IFNAR1 and IFNAR2), it activates the signaling pathway, leading to the formation of the ISGF3 complex. The complex translocates to the cell nucleus and binds to IFN-stimulated response elements in DNA, thereby activating the expression of luciferase. The luciferase readout represents the activation effect of the signaling pathway, making it suitable for evaluating the in vitro effects of IFNα-related drugs.
