Type I interferons are important innate and adaptive immune response factors. It derivates from infected cells and in turn, induces the cells to create an antimicrobial environment that limits the spread of viral pathogens. During this process, interferons will promote antigen presentation and enhance the function of natural killer cells. Furthermore, it also inhibits pro-inflammatory cytokine production and stimulates antigen-specific T and B cell activation. Type I interferons inculdes interferon alfa and interferon beta. Here, we will remarkably introduce Interferon alfa (IFN-α). Interferon alfa is mainly expressed specifically in hematopoietic cells, especially plasmacytoid dendritic cells. Research on the mechanism of action of interferon alfa is a potential breakthrough point in Hepatitis C and Hairy cell leukemia (HCL) research.
Interferon alfa is an important immune factor with antiviral function.
The downstream gene enrichment of Interferon alfa further exerts potent antiviral and anti-proliferative activities on target cells. Interferon alfa binds the IFN-α receptor (IFNAR), targeting the IFNAR1 and IFNAR2 subunits for signaling. Instead, IFNAR goes on to activate the protein tyrosine kinases Janus kinase 1 (JAK1) and tyrosine kinase 2 (TYK2) and phosphorylates Stat1 and Stat2. Interferon alfa will form a heterodimer with Stat1 and Stat2, which subsequently binds to the DNA-binding protein IRF-9 (p48) and forms ISGF-3 (IFN-stimulated gene factor 3). ISGF-3 binds the IFN-stimulated response element (ISRE), activating ISG transcription. ISGs encode proteins that inhibit viral transcription, translation and replication, and degradation of viral nucleic acids.
Altogether, Interferon alfa is mainly produced in innate immune cells, enhances antigen presentation, and upregulates immune cytokines. It controls innate and adaptive immunity as well as intracellular antimicrobial programs.