Interleukin 23

Interleukin 23, alpha subunit p19, also known as IL23A, is a human gene.cite web | title = Entrez Gene: IL23A interleukin 23, alpha subunit p19| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=51561| accessdate = ]

PBB_Summary
section_title =
summary_text = This gene encodes a subunit of the heterodimeric cytokine interleukin 23 (IL23). IL23 is composed of this protein and the p40 subunit of interleukin 12 (IL12B). The receptor of IL23 is formed by the beta 1 subunit of IL12 (IL12RB1) and an IL23 specific subunit, IL23R. Both IL23 and IL12 can activate the transcription activator STAT4, and stimulate the production of interferon-gamma (IFNG). In contrast to IL12, which acts mainly on naive CD4(+) T cells, IL23 preferentially acts on memory CD4(+) T cells.cite web | title = Entrez Gene: IL23A interleukin 23, alpha subunit p19| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=51561| accessdate = ]

Interleukin-23 (IL-23) is a heterodimeric cytokine consisting of two subunits, one called p40, which is shared with another cytokine, IL-12, and another called p19 (the IL-23 alpha subunit). IL-23 is an important part of the inflammatory response against infection. It promotes upregulation of the matrix metalloprotease MMP9, increases angiogenesis and reduces CD8+ T-cell infiltration. Recently, IL-23 has been implicated in the development of cancerous tumors. In conjunction with IL-6 and TGF-β1, IL-23 stimulates naive CD4+ T cells to differentiate into a novel subset of cells called Th17 cells, which are distinct from the classical Th1 and Th2 cells. Th17 cells produce IL-17, a proinflammatory cytokine that enhances T cell priming and stimulates the production of proinflammatory molecules such as IL-1, IL-6, TNF-alpha, NOS-2, and chemokines resulting in inflammation. Knockout mice deficient in either p40 or p19, or in either subunit of the IL-23 receptor (IL-23R and IL12R-β1) develop less severe symptoms of multiple sclerosis and inflammatory bowel disease highlighting the importance of IL-23 in the inflammatory pathway.cite journal | author = Langowski JL, Zhang X, Wu L, Mattson JD, Chen T, Smith K, Basham B, McClanahan T, Kastelein RA, Oft M | title = IL-23 promotes tumour incidence and growth | journal = Nature | volume = 442 | issue = 7101 | pages = 461–5 | year = 2006 | pmid = 16688182 | doi = 10.1038/nature04808 | issn = ] cite journal | author = Kikly K, Liu L, Na S, Sedgwick JD | title = The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation | journal = Curr. Opin. Immunol. | volume = 18 | issue = 6 | pages = 670–5 | year = 2006 | pmid = 17010592 | doi = 10.1016/j.coi.2006.09.008 | issn = ]

ee also

* CNTO 1275, an experimental therapeutic anti-IL-23 antibody

References

Further reading

PBB_Further_reading
citations =
*cite journal | author=Lankford CS, Frucht DM |title=A unique role for IL-23 in promoting cellular immunity. |journal=J. Leukoc. Biol. |volume=73 |issue= 1 |pages= 49–56 |year= 2003 |pmid= 12525561 |doi=
*cite journal | author=van de Vosse E, Lichtenauer-Kaligis EG, van Dissel JT, Ottenhoff TH |title=Genetic variations in the interleukin-12/interleukin-23 receptor (beta1) chain, and implications for IL-12 and IL-23 receptor structure and function. |journal=Immunogenetics |volume=54 |issue= 12 |pages= 817–29 |year= 2003 |pmid= 12671732 |doi= 10.1007/s00251-002-0534-9
*cite journal | author=Kreymborg K, Böhlmann U, Becher B |title=IL-23: changing the verdict on IL-12 function in inflammation and autoimmunity. |journal=Expert Opin. Ther. Targets |volume=9 |issue= 6 |pages= 1123–36 |year= 2006 |pmid= 16300465 |doi= 10.1517/14728222.9.6.1123
*cite journal | author=Peluso I, Pallone F, Monteleone G |title=Interleukin-12 and Th1 immune response in Crohn's disease: pathogenetic relevance and therapeutic implication. |journal=World J. Gastroenterol. |volume=12 |issue= 35 |pages= 5606–10 |year= 2006 |pmid= 17007011 |doi=
*cite journal | author=Prashar Y, Weissman SM |title=Analysis of differential gene expression by display of 3' end restriction fragments of cDNAs. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue= 2 |pages= 659–63 |year= 1996 |pmid= 8570611 |doi=
*cite journal | author=Oppmann B, Lesley R, Blom B, "et al." |title=Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. |journal=Immunity |volume=13 |issue= 5 |pages= 715–25 |year= 2001 |pmid= 11114383 |doi=
*cite journal | author=Wiekowski MT, Leach MW, Evans EW, "et al." |title=Ubiquitous transgenic expression of the IL-23 subunit p19 induces multiorgan inflammation, runting, infertility, and premature death. |journal=J. Immunol. |volume=166 |issue= 12 |pages= 7563–70 |year= 2001 |pmid= 11390512 |doi=
*cite journal | author=Parham C, Chirica M, Timans J, "et al." |title=A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rbeta1 and a novel cytokine receptor subunit, IL-23R. |journal=J. Immunol. |volume=168 |issue= 11 |pages= 5699–708 |year= 2002 |pmid= 12023369 |doi=
*cite journal | author=Broberg EK, Setälä N, Erälinna JP, "et al." |title=Herpes simplex virus type 1 infection induces upregulation of interleukin-23 (p19) mRNA expression in trigeminal ganglia of BALB/c mice. |journal=J. Interferon Cytokine Res. |volume=22 |issue= 6 |pages= 641–51 |year= 2003 |pmid= 12162874 |doi= 10.1089/10799900260100123
*cite journal | author=Pirhonen J, Matikainen S, Julkunen I |title=Regulation of virus-induced IL-12 and IL-23 expression in human macrophages. |journal=J. Immunol. |volume=169 |issue= 10 |pages= 5673–8 |year= 2003 |pmid= 12421946 |doi=
*cite journal | author=Strausberg RL, Feingold EA, Grouse LH, "et al." |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899–903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899
*cite journal | author=Lo CH, Lee SC, Wu PY, "et al." |title=Antitumor and antimetastatic activity of IL-23. |journal=J. Immunol. |volume=171 |issue= 2 |pages= 600–7 |year= 2003 |pmid= 12847224 |doi=
*cite journal | author=Clark HF, Gurney AL, Abaya E, "et al." |title=The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment. |journal=Genome Res. |volume=13 |issue= 10 |pages= 2265–70 |year= 2003 |pmid= 12975309 |doi= 10.1101/gr.1293003
*cite journal | author=Lee E, Trepicchio WL, Oestreicher JL, "et al." |title=Increased expression of interleukin 23 p19 and p40 in lesional skin of patients with psoriasis vulgaris. |journal=J. Exp. Med. |volume=199 |issue= 1 |pages= 125–30 |year= 2004 |pmid= 14707118 |doi= 10.1084/jem.20030451
*cite journal | author=Verreck FA, de Boer T, Langenberg DM, "et al." |title=Human IL-23-producing type 1 macrophages promote but IL-10-producing type 2 macrophages subvert immunity to (myco)bacteria. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=101 |issue= 13 |pages= 4560–5 |year= 2004 |pmid= 15070757 |doi= 10.1073/pnas.0400983101
*cite journal | author=Smits HH, van Beelen AJ, Hessle C, "et al." |title=Commensal Gram-negative bacteria prime human dendritic cells for enhanced IL-23 and IL-27 expression and enhanced Th1 development. |journal=Eur. J. Immunol. |volume=34 |issue= 5 |pages= 1371–80 |year= 2004 |pmid= 15114670 |doi= 10.1002/eji.200324815
*cite journal | author=Schnurr M, Toy T, Shin A, "et al." |title=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. |journal=Blood |volume=105 |issue= 4 |pages= 1582–9 |year= 2005 |pmid= 15486065 |doi= 10.1182/blood-2004-05-1718
*cite journal | author=Gerhard DS, Wagner L, Feingold EA, "et al." |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504

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