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Gene Symbol |
IL27 |
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Aliases |
IL-27, IL-27A, IL27A, IL27p28, IL30, p28 |
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Entrez Gene ID |
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Gene Name |
Interleukin 27 |
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Chromosomal Location |
16p12.1-p11.2 |
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HGNC ID |
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Summary |
The protein encoded by this gene is one of the subunits of a heterodimeric cytokine complex. This protein is related to interleukin 12A (IL12A). It interacts with Epstein-Barr virus induced gene 3 (EBI3), a protein similar to interleukin 12B (IL12B), and forms a complex that has been shown to drive rapid expansion of naive but not memory CD4(+) T cells. The complex is also found to synergize strongly with interleukin 12 to trigger interferon gamma (IFNG) production of naive CD4(+) T cells. The biological effects of this cytokine are mediated by the class I cytokine receptor (WSX1/TCRR). [provided by RefSeq, Jul 2008]
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e!Ensembl
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Protein Information |
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Protein Name |
Interleukin-27 subunit alpha, IL-27 p28 subunit, IL-27 subunit alpha, IL-27-A, IL27-A, interleukin-30 |
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Function |
Associates with EBI3 to form the IL-27 interleukin, a heterodimeric cytokine which functions in innate immunity. IL-27 has pro- and anti-inflammatory properties, that can regulate T-helper cell development, suppress T-cell proliferation, stimulate cytotoxic T-cell activity, induce isotype switching in B-cells, and that has diverse effects on innate immune cells. Among its target cells are CD4 T-helper cells which can differentiate in type 1 effector cells (TH1), type 2 effector cells (TH2) and IL17 producing helper T-cells (TH17). It drives rapid clonal expansion of naive but not memory CD4 T-cells. It also strongly synergizes with IL-12 to trigger interferon-gamma/IFN-gamma production of naive CD4 T-cells, binds to the cytokine receptor WSX-1/TCCR which appears to be required but not sufficient for IL-27-mediated signal transduction. IL-27 potentiate the early phase of TH1 response and suppress TH2 and TH17 differentiation. It induces the differentiation of TH1 cells via two distinct pathways, p38 MAPK/TBX21- and ICAM1/ITGAL/ERK-dependent pathways. It also induces STAT1, STAT3, STAT4 and STAT5 phosphorylation and activates TBX21/T-Bet via STAT1 with resulting IL12RB2 up-regulation, an event crucial to TH1 cell commitment. It suppresses the expression of GATA3, the inhibitor TH1 cells development. In CD8 T-cells, it activates STATs as well as GZMB. IL-27 reveals to be a potent inhibitor of TH17 cell development and of IL-17 production. Indeed IL27 alone is also able to inhibit the production of IL17 by CD4 and CD8 T-cells. While IL-27 suppressed the development of proinflammatory Th17 cells via STAT1, it inhibits the development of anti-inflammatory inducible regulatory T-cells, iTreg, independently of STAT1. IL-27 has also an effect on cytokine production, it suppresses proinflammatory cytokine production such as IL2, IL4, IL5 and IL6 and activates suppressors of cytokine signaling such as SOCS1 and SOCS3. Apart from suppression of cytokine production, IL-27 also antagonizes the effects of some cytokines such as IL6 through direct effects on T-cells. Another important role of IL-27 is its antitumor activity as well as its antiangiogenic activity with activation of production of antiangiogenic chemokines such as IP-10/CXCL10 and MIG/CXCL9. In vein endothelial cells, it induces IRF1/interferon regulatory factor 1 and increase the expression of MHC class II transactivator/CIITA with resulting up-regulation of major histocompatibility complex class II. IL-27 also demonstrates antiviral activity with inhibitory properties on HIV-1 replication. |
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UniProt |
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Interactions |
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STRING |
MINT |
IntAct |
ENSP00000454071 |
P01130 |
P01130 |
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View interactions
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Associated Diseases
Disease group | Disease Name | References |
Digestive System Diseases |
Cholangitis |
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Crohn Disease |
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Inflammatory Bowel Diseases |
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Colitis |
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Endocrine System Diseases |
Diabetes Mellitus |
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Ketosis-prone diabetes |
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Brittle diabetes |
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PCOS |
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Immune System Diseases |
Autoimmune Diabetes |
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Musculoskeletal Diseases |
Spondylitis |
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Neoplasms |
Prostate cancer |
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Skin and Connective Tissue Diseases |
Psoriasis |
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References |
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Nehir Aytan Asli, Bastu Ercan, Demiral Irem, Bulut Huri, Dogan Murat, Buyru Faruk |
a Department of Obstetrics and Gynecology , Istanbul University School of Medicine , Istanbul , Turkey and.| a Department of Obstetrics and Gynecology , Istanbul University School of Medicine , Istanbul , Turkey and.| a Department of Obstetrics and Gynecology , Istanbul University School of Medicine , Istanbul , Turkey and.| b Department of Biochemistry , Bezmialem Foundation University, Faculty of Science , Istanbul , Turkey.| a Department of Obstetrics and Gynecology , Istanbul University School of Medicine , Istanbul , Turkey and.| a Department of Obstetrics and Gynecology , Istanbul University School of Medicine , Istanbul , Turkey and. |
Gynecol Endocrinol. 2016 Sep;32(9):709-713. doi: 10.3109/09513590.2016.1155208. |
Abstract
This prospective study aimed to determine the status of circulating levels of C-reactive protein (CRP), tumor necrosis factor alpha (TNF-alpha), IL-27, IL-35, IL-37, alpha-1 acid glycoprotein in patients with polycystic ovary syndrome (PCOS) compared with controls and to evaluate their relation with hyperandrogenism and obesity. Forty-eight patients with PCOS (29 obese, 19 lean) and 40 healthy controls (20 obese, 20 lean) were enrolled. CRP, TNF-alpha, IL-27, IL-35, IL-37, alpha-1 acid glycoprotein, sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEA-S) levels were measured. Levels of total testosterone, A4, DHEA-S were significantly higher in patients with PCOS than in controls both in the obese and lean groups, while levels of SHBG were significantly lower in all patients with PCOS than in all (p < 0.05). Free androgen index (FAI) values were significantly higher in all patients with PCOS than in all controls (all p < 0.05). Levels of CRP, TNF-alpha, alpha-1 acid glycoprotein were significantly increased in all patients with PCOS compared with all controls (all p < 0.001). FAI had a positive correlation with CRP, TNF-alpha, alpha-1 acid glycoprotein, a negative correlation with IL-27, IL-25, IL-37 (all p < 0.01). Body mass index had a negative correlation with IL-27, IL-35, IL-37, a positive correlation with alpha-1 acid glycoprotein, FAI (p < 0.05). The findings confirm the proinflammatory state of PCOS. Moreover, obesity along with PCOS significantly elevates the inflammatory status and hyperandrogenism. |
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