Cited 113 times in
Genetic polymorphisms of IL-23R and IL-17A and novel insights into their associations with inflammatory bowel disease
DC Field | Value | Language |
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dc.contributor.author | 문창모 | - |
dc.contributor.author | 박재준 | - |
dc.contributor.author | 천재희 | - |
dc.contributor.author | 김승원 | - |
dc.contributor.author | 김원호 | - |
dc.contributor.author | 김은수 | - |
dc.contributor.author | 김태일 | - |
dc.date.accessioned | 2014-12-20T17:13:27Z | - |
dc.date.available | 2014-12-20T17:13:27Z | - |
dc.date.issued | 2011 | - |
dc.identifier.issn | 0017-5749 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/94191 | - |
dc.description.abstract | BACKGROUND AND AIMS: To identify the associations of genetic and epigenetic variations in IL-23R and IL-17A with inflammatory bowel diseases (IBD). METHODS: The promoter and exon regions of IL-23R and IL-17A were analysed in 727 subjects (201 Crohn's disease, 268 ulcerative colitis and 258 healthy controls) using DNA sequencing and denaturing high performance liquid chromatography. Transcription factor binding affinity, IL-17A mRNA expression and methylation of the IL-17A promoter were evaluated in peripheral blood mononuclear cells (PBMC) and Jurkat cells. RESULTS: A case-control analysis showed that development of Crohn's disease is associated with the IL-23R variant G149R (OR 0.32, 95% CI 0.15 to 0.68) and IL-17A variant IVS1+18G>C (OR 10.65, 95% CI 1.32 to 85.89). Ulcerative colitis patients showed an association with IL-23R variants G149R (OR 0.41, 95% CI 0.21 to 0.76), IVS4+17C>T (OR 2.89, 95% CI 1.20 to 6.96) and Q3H (OR 0.61, 95% CI 0.38 to 0.99), and IL-17A variants -737C>T (OR 1.50, 95% CI 1.06 to 2.13), -197G>A (OR 0.63, 95% CI 0.40 to 0.97) and IVS1+18 G>C (OR 8.93, 95% CI 1.12 to 70.99). The -877G, -737T and -444A risk alleles of IL-17A displayed higher binding affinities with the transcription factor complex and higher expression levels of IL-17A transcripts. DNA hypomethylation of the IL-17A promoter was observed in PBMC from IBD patients with a significant inverse correlation between methylation extent of IVS1+17 and IL-17A mRNA level. Finally, Jurkat cells recovered IL-17A mRNA expression after exposure to demethylating agent. CONCLUSIONS: The results provide insights into the genetic and epigenetic interactions in the IL-23R/IL-17 axis that are associated with elevated expression of IL-17 and IBD pathogenesis. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 1527~1536 | - |
dc.relation.isPartOf | GUT | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Asian Continental Ancestry Group/genetics* | - |
dc.subject.MESH | Case-Control Studies | - |
dc.subject.MESH | Chromatography, High Pressure Liquid | - |
dc.subject.MESH | Colitis, Ulcerative/ethnology | - |
dc.subject.MESH | Colitis, Ulcerative/genetics* | - |
dc.subject.MESH | Crohn Disease/ethnology | - |
dc.subject.MESH | Crohn Disease/genetics* | - |
dc.subject.MESH | DNA Methylation | - |
dc.subject.MESH | Electrophoretic Mobility Shift Assay | - |
dc.subject.MESH | Epigenesis, Genetic | - |
dc.subject.MESH | Exons/genetics | - |
dc.subject.MESH | Genetic Predisposition to Disease/genetics* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Interleukin-17* | - |
dc.subject.MESH | Polymorphism, Single Nucleotide | - |
dc.subject.MESH | Promoter Regions, Genetic/genetics | - |
dc.subject.MESH | Receptors, Interleukin/genetics* | - |
dc.subject.MESH | Receptors, Interleukin-17/genetics* | - |
dc.title | Genetic polymorphisms of IL-23R and IL-17A and novel insights into their associations with inflammatory bowel disease | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Seung Won Kim | - |
dc.contributor.googleauthor | Eun Soo Kim | - |
dc.contributor.googleauthor | Chang Mo Moon | - |
dc.contributor.googleauthor | Jae Jun Park | - |
dc.contributor.googleauthor | Tae Il Kim | - |
dc.contributor.googleauthor | Won Ho Kim | - |
dc.contributor.googleauthor | Jae Hee Cheon | - |
dc.identifier.doi | 10.1136/gut.2011.238477 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01390 | - |
dc.contributor.localId | A01636 | - |
dc.contributor.localId | A00774 | - |
dc.contributor.localId | A01079 | - |
dc.contributor.localId | A04030 | - |
dc.contributor.localId | A00804 | - |
dc.contributor.localId | A00656 | - |
dc.relation.journalcode | J00953 | - |
dc.identifier.eissn | 1468-3288 | - |
dc.identifier.pmid | 21672939 | - |
dc.identifier.url | http://gut.bmj.com/content/60/11/1527 | - |
dc.subject.keyword | Genetic polymorphism | - |
dc.subject.keyword | IL-17A | - |
dc.subject.keyword | IL-23R | - |
dc.subject.keyword | inflammatory bowel disease | - |
dc.contributor.alternativeName | Moon, Chang Mo | - |
dc.contributor.alternativeName | Park, Jae Jun | - |
dc.contributor.alternativeName | Cheon, Jae Hee | - |
dc.contributor.alternativeName | Kim, Seung Won | - |
dc.contributor.alternativeName | Kim, Won Ho | - |
dc.contributor.alternativeName | Kim, Eun Soo | - |
dc.contributor.alternativeName | Kim, Tae Il | - |
dc.contributor.affiliatedAuthor | Moon, Chang Mo | - |
dc.contributor.affiliatedAuthor | Park, Jae Jun | - |
dc.contributor.affiliatedAuthor | Kim, Won Ho | - |
dc.contributor.affiliatedAuthor | Kim, Tae Il | - |
dc.contributor.affiliatedAuthor | Cheon, Jae Hee | - |
dc.contributor.affiliatedAuthor | Kim, Eun Soo | - |
dc.contributor.affiliatedAuthor | Kim, Seung Won | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 60 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 1527 | - |
dc.citation.endPage | 1536 | - |
dc.identifier.bibliographicCitation | GUT, Vol.60(11) : 1527-1536, 2011 | - |
dc.identifier.rimsid | 27301 | - |
dc.type.rims | ART | - |
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