Interleukin-26 (IL-26) is a protein that in humans is encoded by the IL26gene.[1][2][3]
IL-26 is a 171-amino acid protein, which is similar in amino acid sequence to interleukin 10. It was originally called AK155 and is composed of a signal sequence, 6 helices, and 4 conserved cysteine residues. IL-26 is expressed in certain herpesvirus-transformed T cells but not in primary stimulated T cells.[2] IL-26 signals through a receptor complex comprising two distinct proteins called IL-20 receptor 1 and IL-10 receptor 2.[4] By signaling through this receptor complex, IL-26 induces rapid phosphorylation of the transcription factors STAT1 and STAT3, which enhance IL-10 and IL-8 secretion and as expression of the CD54 molecule on the surface of epithelial cells.[5]
Role
Interleukin 26 (IL-26), is a natural human antimicrobial that promotes immune sensing of bacterial and host cell death. IL-26, a human TH17 cell–derived cytokine, is a cationic amphipathic protein that kills extracellular bacteria via membrane-pore formation. Furthermore, TH17 cell–derived IL-26 formed complexes with bacterial DNA and self-DNA released by dying bacteria and host cells. The IL-26–DNA complexes triggered the production of type I interferon by plasmacytoid dendritic cells via activation of Toll-like receptor 9, but independently of the IL-26 receptor.[6]
↑Goris A, Marrosu MG, Vandenbroeck K (August 2001). "Novel polymorphisms in the IL-10 related AK155 gene (chromosome 12q15)". Genes Immun. 2 (5): 284–6. doi:10.1038/sj.gene.6363772. PMID11528524.
↑Sheikh F, Baurin VV, Lewis-Antes A, Shah NK, Smirnov SV, Anantha S, Dickensheets H, Dumoutier L, Renauld JC, Zdanov A, Donnelly RP, Kotenko SV (February 2004). "Cutting edge: IL-26 signals through a novel receptor complex composed of IL-20 receptor 1 and IL-10 receptor 2". J. Immunol. 172 (4): 2006–10. doi:10.4049/jimmunol.172.4.2006. PMID14764663.
↑Hör S, Pirzer H, Dumoutier L, Bauer F, Wittmann S, Sticht H, Renauld J, de Waal Malefyt R, Fickenscher H (2004). "The T-cell lymphokine interleukin-26 targets epithelial cells through the interleukin-20 receptor 1 and interleukin-10 receptor 2 chains". J Biol Chem. 279 (32): 33343–51. doi:10.1074/jbc.M405000200. PMID15178681.
Davila S, Froeling FE, Tan A, et al. (2010). "New genetic associations detected in a host response study to hepatitis B vaccine". Genes Immun. 11 (3): 232–8. doi:10.1038/gene.2010.1. PMID20237496.
Dambacher J, Beigel F, Zitzmann K, et al. (2009). "The role of the novel Th17 cytokine IL-26 in intestinal inflammation". Gut. 58 (9): 1207–17. doi:10.1136/gut.2007.130112. PMID18483078.
Sheikh F, Baurin VV, Lewis-Antes A, et al. (2004). "Cutting edge: IL-26 signals through a novel receptor complex composed of IL-20 receptor 1 and IL-10 receptor 2". J. Immunol. 172 (4): 2006–10. doi:10.4049/jimmunol.172.4.2006. PMID14764663.
Siezen CL, Bont L, Hodemaekers HM, et al. (2009). "Genetic susceptibility to respiratory syncytial virus bronchiolitis in preterm children is associated with airway remodeling genes and innate immune genes". Pediatr. Infect. Dis. J. 28 (4): 333–5. doi:10.1097/INF.0b013e31818e2aa9. PMID19258923.
Vandenbroeck K, Cunningham S, Goris A, et al. (2003). "Polymorphisms in the interferon-gamma/interleukin-26 gene region contribute to sex bias in susceptibility to rheumatoid arthritis". Arthritis Rheum. 48 (10): 2773–8. doi:10.1002/art.11236. PMID14558082.
Dumoutier L, Van Roost E, Ameye G, et al. (2000). "IL-TIF/IL-22: genomic organization and mapping of the human and mouse genes". Genes Immun. 1 (8): 488–94. doi:10.1038/sj.gene.6363716. PMID11197690.
Schuurhof A, Bont L, Siezen CL, et al. (2010). "Interleukin-9 polymorphism in infants with respiratory syncytial virus infection: an opposite effect in boys and girls". Pediatr. Pulmonol. 45 (6): 608–13. doi:10.1002/ppul.21229. PMID20503287.
Meller, S., Di Domizio, J., Voo, K. S., Friedrich, H. C., Chamilos, G., Ganguly, D., ... & Ladbury, J. E. (2015). TH17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26. Nature immunology, 16(9), 970-979.
