Interleukin 23

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Interleukin 23, alfa podjedinica p19
Identifikatori
SimboliIL23A; P19; IL-23; IL-23A; IL23P19; MGC79388; SGRF
Vanjski IDOMIM: 605580 MGI: 1932410 HomoloGene: 12832 GeneCards: IL23A Gene
Pregled RNK izražavanja
podaci
Ortolozi
VrstaČovekMiš
Entrez5156183430
EnsemblENSG00000110944ENSMUSG00000025383
UniProtQ9NPF7Q9EQ14
Ref. Sekv. (iRNK)NM_016584NM_031252
Ref. Sekv. (protein)NP_057668NP_112542
Lokacija (UCSC)Chr 12:
55.02 - 55.02 Mb		Chr 10:
127.7 - 127.7 Mb
PubMed pretraga[1][2]

Interleukin 23 podjedinica alfa je protein koji je kod ljudi kodira IL23A gen.[1][2][3][4]

Ovaj gen kodira p19 podjedinicu heterodimerskog citokina interleukin 23 (IL23). IL23 se sastoji od ovog proteina i p40 podjedinice interleukina 12 (IL12B). IL23 receptor je formiran od beta 1 podjedinice IL12 (IL12RB1) i IL23 specifične podjedinice, IL23R. Oba interleukina, IL23 i IL12, mogu aktivirati traskripcioni aktivator STAT4, i stimulisati produkciju interferona gama (INFG). U kontrastu sa IL12, koje deluje uglavnom na naivnim CD4(+) T ćelijama, IL23 preferentno deluje na memorijske CD4(+) T ćelije.[2]

IL-23 je važan deo inflamatornog odgovora na infekciju. On podstiče izražavanje matriks metaloproteaza MMP9, povećava angiogenezu i redukuje infiltraciju CD8+ T-ćelija. Nedavno, IL-23 je bio impliciran u razvoj kancerogenih tumora. U kombinaciji sa IL-6 i TGF-β1, IL-23 stimuliše naivne CD4+ T ćelije da se diferenciraju u nove podskupove ćelija koje se zovu Th17 ćelije, koje se razlikuju od klasičnih Th1 i Th2 ćelija. Th17 ćelije proizvode IL-17, proinflamatorni citokin koji pojačava T ćelijsko oformljavanje i stimuliše produkciju proinflamatornih molekula kao što su IL-1, IL-6, TNF-alfa, NOS-2, i hemokine rezultujući u inflamaciji. Nokaut miševi deficitni u bilo p40 ili p19, ili u bilo kojoj podjedinici IL-23 receptora (IL-23R i IL12R-β1) razvijaju manje ozbiljne simptome multiple skleroze i upalne bolesti creva naglašavajući važnost IL-23 u inflamatornom putu.[5][6]

Interakcije

Za interleukin 23 je bilo pokazano da ostvaruje interakcije sa Interleukin-12 podjedinicom beta.[7]

Povezano

  • CNTO 1275, eksperimentalni terapeutsko anti-IL-23 antitelo

Reference

  1. ↑ Oppmann B, Lesley R, Blom B, Timans JC, Xu Y, Hunte B, Vega F, Yu N, Wang J, Singh K, Zonin F, Vaisberg E, Churakova T, Liu M, Gorman D, Wagner J, Zurawski S, Liu Y, Abrams JS, Moore KW, Rennick D, de Waal-Malefyt R, Hannum C, Bazan JF, Kastelein RA (Jan 2001). „Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12”. Immunity 13 (5): 715–25. PMID 11114383. 
  2. ↑ 2,0 2,1 „Entrez Gene: IL23A interleukin 23, alpha subunit p19”. 
  3. ↑ Thomas J. Kindt, Richard A. Goldsby, Barbara Anne Osborne, Janis Kuby (2006). Kuby Immunology (6 izd.). New York: W H Freeman and company. ISBN 1-4292-0211-4. 
  4. ↑ Mire-Sluis, Anthony R.; Thorpe, Robin, ur. (1998). Cytokines (Handbook of Immunopharmacology). Boston: Academic Press. ISBN 0-12-498340-5. 
  5. ↑ Langowski JL, Zhang X, Wu L, Mattson JD, Chen T, Smith K, Basham B, McClanahan T, Kastelein RA, Oft M (2006). „IL-23 promotes tumour incidence and growth”. Nature 442 (7101): 461–5. DOI:10.1038/nature04808. PMID 16688182. 
  6. ↑ Kikly K, Liu L, Na S, Sedgwick JD (2006). „The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation”. Curr. Opin. Immunol. 18 (6): 670–5. DOI:10.1016/j.coi.2006.09.008. PMID 17010592. 
  7. ↑ Oppmann, B; Lesley R, Blom B, Timans J C, Xu Y, Hunte B, Vega F, Yu N, Wang J, Singh K, Zonin F, Vaisberg E, Churakova T, Liu M, Gorman D, Wagner J, Zurawski S, Liu Y, Abrams J S, Moore K W, Rennick D, de Waal-Malefyt R, Hannum C, Bazan J F, Kastelein R A (2000). „Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12”. Immunity (UNITED STATES) 13 (5): 715–25. ISSN 1074-7613. PMID 11114383. 

Literatura

  • Lankford CS, Frucht DM (2003). „A unique role for IL-23 in promoting cellular immunity.”. J. Leukoc. Biol. 73 (1): 49–56. DOI:10.1189/jlb.0602326. PMID 12525561. 
  • van de Vosse E, Lichtenauer-Kaligis EG, van Dissel JT, Ottenhoff TH (2003). „Genetic variations in the interleukin-12/interleukin-23 receptor (beta1) chain, and implications for IL-12 and IL-23 receptor structure and function.”. Immunogenetics 54 (12): 817–29. DOI:10.1007/s00251-002-0534-9. PMID 12671732. 
  • Kreymborg K, Böhlmann U, Becher B (2006). „IL-23: changing the verdict on IL-12 function in inflammation and autoimmunity.”. Expert Opin. Ther. Targets 9 (6): 1123–36. DOI:10.1517/14728222.9.6.1123. PMID 16300465. 
  • Peluso I, Pallone F, Monteleone G (2006). „Interleukin-12 and Th1 immune response in Crohn's disease: pathogenetic relevance and therapeutic implication.”. World J. Gastroenterol. 12 (35): 5606–10. PMID 17007011. 
  • Prashar Y, Weissman SM (1996). „Analysis of differential gene expression by display of 3' end restriction fragments of cDNAs.”. Proc. Natl. Acad. Sci. U.S.A. 93 (2): 659–63. DOI:10.1073/pnas.93.2.659. PMID 8570611. 
  • Wiekowski MT, Leach MW, Evans EW, et al. (2001). „Ubiquitous transgenic expression of the IL-23 subunit p19 induces multiorgan inflammation, runting, infertility, and premature death.”. J. Immunol. 166 (12): 7563–70. PMID 11390512. 
  • Parham C, Chirica M, Timans J, et al. (2002). „A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rbeta1 and a novel cytokine receptor subunit, IL-23R.”. J. Immunol. 168 (11): 5699–708. PMID 12023369. 
  • Broberg EK, Setälä N, Erälinna JP, et al. (2003). „Herpes simplex virus type 1 infection induces upregulation of interleukin-23 (p19) mRNA expression in trigeminal ganglia of BALB/c mice.”. J. Interferon Cytokine Res. 22 (6): 641–51. DOI:10.1089/10799900260100123. PMID 12162874. 
  • Pirhonen J, Matikainen S, Julkunen I (2003). „Regulation of virus-induced IL-12 and IL-23 expression in human macrophages.”. J. Immunol. 169 (10): 5673–8. PMID 12421946. 
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). „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. PMID 12477932. 
  • Lo CH, Lee SC, Wu PY, et al. (2003). „Antitumor and antimetastatic activity of IL-23.”. J. Immunol. 171 (2): 600–7. PMID 12847224. 
  • Clark HF, Gurney AL, Abaya E, et al. (2003). „The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment.”. Genome Res. 13 (10): 2265–70. DOI:10.1101/gr.1293003. PMID 12975309. 
  • Lee E, Trepicchio WL, Oestreicher JL, et al. (2004). „Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris.”. J. Exp. Med. 199 (1): 125–30. DOI:10.1084/jem.20030451. PMID 14707118. 
  • Verreck FA, de Boer T, Langenberg DM, et al. (2004). „Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco)bacteria.”. Proc. Natl. Acad. Sci. U.S.A. 101 (13): 4560–5. DOI:10.1073/pnas.0400983101. PMID 15070757. 
  • Smits HH, van Beelen AJ, Hessle C, et al. (2004). „Commensal Gram-negative bacteria prime human dendritic cells for enhanced IL-23 and IL-27 expression and enhanced Th1 development.”. Eur. J. Immunol. 34 (5): 1371–80. DOI:10.1002/eji.200324815. PMID 15114670. 
  • Schnurr M, Toy T, Shin A, et al. (2005). „Extracellular nucleotide signaling by P2 receptors inhibits IL-12 and enhances IL-23 expression in human dendritic cells: a novel role for the cAMP pathway.”. Blood 105 (4): 1582–9. DOI:10.1182/blood-2004-05-1718. PMID 15486065. 
  • 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. PMID 15489334. 

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