Interferon alpha 8 (IFNA8) also known as leukocyte interferon, represents a group of related but distinct proteins that share over 95% amino acid s equence homology. They are members of the type I interferon family which share a common cell surface receptor composed of two subunits, a 100 kDa ligand-binding subunit (IFN-alpha R2) and a 125 kDa ligand binding and signal transduction subunit (IFN-alpha R1) that is involved both in ligand binding and signal transduction. IFN-alpha has both anti-viral and immunomodulatory activities on target cells.Interferons (IFN) are a family of cytokines with potent antiviral, antiproliferative and immunomodulatory properties, classified based on their binding specificity to cell surface receptors [1]. Human IFNA2 was originally cloned in the early 80s and now more than a dozen closely related IFN alpha subtypes have been identified in both the human and mouse genome, each sharing about 80% amino acid (aa) sequence homology [2-4]. Structurally, type I IFNs belong to the class of five helical-bundle cytokines, with the IFNA subtypes containing 2 conserved disulfide bonds [5]. The extracellular domain (ECD) of mature human IFNA8, also known as IFN-alpha B2, shares 60% aa sequence identity with mouse homolog. The type I IFNs bind to the interferon alpha receptor (IFNAR), which consists of two subunits: IFNAR1 (alpha-subunit) and IFNAR2 (beta -subunit) [6, 7]. Individual IFNA subtypes are known to display unique efficacies to viral protection, and IFNA8 is the most potent IFNA, judging by both antiviral and antiproliferative activities [8].
Reference
[1]. Pestka, S. et al. (1987) Annu. Rev. Biochem. 56:727.
[2]. Goeddel, D.V. et al. (1980) Nature 287:411.
[3]. Matsumiya, T. et al. (2007) J. Immunol. 179:4542.
[4]. Schreiber, G. and J. Piehler (2015) Trends Immunol. 36:139.
[5]. Wittling, M.C. et al. (2021) Front Immunol. 11:605673.
[6]. van Pesch, V. et al. (2004) J. Virol. 78:8219.
[7]. James, C.M. et al. (2007) Vaccine. 25(10):1856.
[8]. Slutzki, M. et al. (2006) J Mol Biol. 360:1019.