Interleukin 26

IL26
Identifiers
Aliases	IL26, AK155, IL-26, interleukin 26
External IDs	OMIM: 605679 HomoloGene: 81862 GeneCards: IL26
Genetically Related Diseases
ulcerative colitis[1]
Gene ontology Molecular function • cytokine activity Cellular component • extracellular space • extracellular region • cytosol Biological process • cell-cell signaling • positive regulation of cytokine secretion • positive regulation of protein kinase B signaling • inflammatory response • positive regulation of JAK-STAT cascade • immune response • positive regulation of transcription from RNA polymerase II promoter • positive regulation of stress-activated MAPK cascade • positive regulation of ERK1 and ERK2 cascade • negative regulation of epithelial cell proliferation Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	55801	n/a
Ensembl	ENSG00000111536	n/a
UniProt	Q9NPH9	n/a
RefSeq (mRNA)	NM_018402	n/a
RefSeq (protein)	NP_060872.1	n/a
Location (UCSC)	Chr 12: 68.2 – 68.23 Mb	n/a
PubMed search	[2]	n/a
Wikidata

View/Edit Human

Interleukin-26 (IL-26) is a protein that in humans is encoded by the IL26 gene.^[3][4][5]

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.^[4] IL-26 signals through a receptor complex comprising two distinct proteins called IL-20 receptor 1 and IL-10 receptor 2.^[6] 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.^[7]

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.^[8]

References

1. "Diseases that are genetically associated with IL26 view/edit references on wikidata".
2. "Human PubMed Reference:".
3. "Entrez Gene: interleukin 26".
4. Knappe A, Hör S, Wittmann S, Fickenscher H (April 2000). "Induction of a novel cellular homolog of interleukin-10, AK155, by transformation of T lymphocytes with herpesvirus saimiri". J. Virol. 74 (8): 3881–7. doi:10.1128/JVI.74.8.3881-3887.2000. PMC 111897. PMID 10729163.
5. 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. PMID 11528524.
6. 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. PMID 14764663.
7. 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. PMID 15178681.
8. Meller, Stephan; Di Domizio, Jeremy; Voo, Kui S.; Friedrich, Heike C.; Chamilos, Georgios; Ganguly, Dipyaman; Conrad, Curdin; Gregorio, Josh; Le Roy, Didier (2015-09-01). "T(H)17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26". Nature Immunology. 16 (9): 970–979. doi:10.1038/ni.3211. ISSN 1529-2916. PMC 4776746. PMID 26168081.

Further reading

• 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. PMID 20237496.
• Silverberg MS, Cho JH, Rioux JD, et al. (2009). "Ulcerative colitis-risk loci on chromosomes 1p36 and 12q15 found by genome-wide association study". Nat. Genet. 41 (2): 216–20. doi:10.1038/ng.275. PMC 2652837. PMID 19122664.
• 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. PMID 18483078.
• Rose JE, Behm FM, Drgon T, et al. (2010). "Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score". Mol. Med. 16 (7–8): 247–53. doi:10.2119/molmed.2009.00159. PMC 2896464. PMID 20379614.
• 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. PMID 14764663.
• 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. PMID 19258923.
• 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. PMID 14558082.
• 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. PMID 11197690.
• Kantarci OH, Hebrink DD, Schaefer-Klein J, et al. (2008). "Interferon gamma allelic variants: sex-biased multiple sclerosis susceptibility and gene expression". Arch. Neurol. 65 (3): 349–57. doi:10.1001/archneurol.2007.66. PMID 18332247.
• Janssen R, Bont L, Siezen CL, et al. (2007). "Genetic susceptibility to respiratory syncytial virus bronchiolitis is predominantly associated with innate immune genes". J. Infect. Dis. 196 (6): 826–34. doi:10.1086/520886. PMID 17703412.
• Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
• Strausberg RL, Feingold EA, Grouse LH, et al. (2002). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
• Wang K, Baldassano R, Zhang H, et al. (2010). "Comparative genetic analysis of inflammatory bowel disease and type 1 diabetes implicates multiple loci with opposite effects". Hum. Mol. Genet. 19 (10): 2059–67. doi:10.1093/hmg/ddq078. PMC 2860894. PMID 20176734.
• 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. PMID 20503287.

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.