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HLA-C*01 is a Risk Factor for Crohn's Disease

DC FieldValueLanguage
dc.contributor.author김원호-
dc.contributor.author김태일-
dc.contributor.author박수정-
dc.contributor.author이민구-
dc.contributor.author정은석-
dc.contributor.author천재희-
dc.contributor.author홍성필-
dc.date.accessioned2017-10-26T07:21:43Z-
dc.date.available2017-10-26T07:21:43Z-
dc.date.issued2016-
dc.identifier.issn1078-0998-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/151930-
dc.description.abstractBACKGROUND: A dysregulated mucosal immune response to the intestinal environment in a genetically susceptible host is hypothesized to be critical to the pathogenesis of Crohn's disease (CD). Therefore, we examined CD-susceptibility genes involved in the immune response through a genome-wide association study and consecutive genotyping of human leukocyte antigens (HLAs) and killer cell immunoglobulin-like receptors. METHODS: An initial genome-wide association study was performed with 275 CD patients and 2369 controls from a Korean population. To validate the loci identified in the genome-wide association study, replication genotyping was performed in a different cohort of 242 CD patients and 1066 controls. Finally, high-resolution genotyping of HLA and killer cell immunoglobulin-like receptor was performed. RESULTS: Four susceptibility loci, a promoter region in tumor necrosis factor (ligand) superfamily member (TNFSF15) and 3 independent regions in HLAs, showed significant associations with CD. Among them, rs114985235 in the intergenic region between HLA-B and HLA-C showed the strongest association, with an increased risk of CD (P = 8.71 × 10; odds ratio, 2.25). HLA typing in this region showed HLA-C*01 to be responsible for the association of CD among 43 HLA-B and HLA-C genotypes identified in the Korean population. However, the interaction of HLA-C with killer cell immunoglobulin-like receptor had little effect on the development of CD. CONCLUSIONS: We newly identified HLA-C*01 as a prominent CD-susceptibility HLA allotype in the Korean population. In addition, these results confirm that genetic variations in immune response genes, such as HLAs and TNFSF15, are important host factors for the pathogenesis of CD.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherLippincott Williams & Wilkins-
dc.relation.isPartOfINFLAMMATORY BOWEL DISEASES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdolescent-
dc.subject.MESHAdult-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHCohort Studies-
dc.subject.MESHCrohn Disease/epidemiology*-
dc.subject.MESHCrohn Disease/genetics*-
dc.subject.MESHFemale-
dc.subject.MESHFollow-Up Studies-
dc.subject.MESHGenetic Predisposition to Disease-
dc.subject.MESHGenome-Wide Association Study*-
dc.subject.MESHGenotype-
dc.subject.MESHHLA-C Antigens/genetics*-
dc.subject.MESHHumans-
dc.subject.MESHMale-
dc.subject.MESHPolymorphism, Single Nucleotide/genetics*-
dc.subject.MESHPrevalence-
dc.subject.MESHRepublic of Korea/epidemiology-
dc.subject.MESHRisk Factors-
dc.subject.MESHTumor Necrosis Factor Ligand Superfamily Member 15/genetics*-
dc.subject.MESHYoung Adult-
dc.titleHLA-C*01 is a Risk Factor for Crohn's Disease-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorJung, Eun Suk-
dc.contributor.googleauthorCheon, Jae Hee-
dc.contributor.googleauthorLee, Ji Hyun-
dc.contributor.googleauthorPark, Soo Jung-
dc.contributor.googleauthorJang, Hui Won-
dc.contributor.googleauthorChung, Sook Hee-
dc.contributor.googleauthorPark, Myoung Hee-
dc.contributor.googleauthorKim, Tai-Gyu-
dc.contributor.googleauthorOh, Heung-Bum-
dc.contributor.googleauthorYang, Suk-Kyun-
dc.contributor.googleauthorPark, Sang Hyoung-
dc.contributor.googleauthorHan, Jae Yong-
dc.contributor.googleauthorHong, Sung Pil-
dc.contributor.googleauthorKim, Tae Il-
dc.contributor.googleauthorKim, Won Ho-
dc.contributor.googleauthorLee, Min Goo-
dc.identifier.doi10.1097/MIB.0000000000000693-
dc.contributor.localIdA01079-
dc.contributor.localIdA01539-
dc.contributor.localIdA02781-
dc.contributor.localIdA03685-
dc.contributor.localIdA04030-
dc.contributor.localIdA04404-
dc.contributor.localIdA00774-
dc.relation.journalcodeJ01060-
dc.identifier.eissn1536-4844-
dc.identifier.pmid26891255-
dc.identifier.urlhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00054725-201604000-00004&LSLINK=80&D=ovft-
dc.subject.keywordCrohn’s disease-
dc.subject.keywordGWAS-
dc.subject.keywordHLA-
dc.subject.keywordinflammatory bowel disease-
dc.contributor.alternativeNameKim, Won Ho-
dc.contributor.alternativeNameKim, Tae Il-
dc.contributor.alternativeNamePark, Soo Jung-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.alternativeNameJung, Eun Suk-
dc.contributor.alternativeNameCheon, Jae Hee-
dc.contributor.alternativeNameHong, Sung Pil-
dc.contributor.affiliatedAuthorKim, Tae Il-
dc.contributor.affiliatedAuthorPark, Soo Jung-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorJung, Eun Suk-
dc.contributor.affiliatedAuthorCheon, Jae Hee-
dc.contributor.affiliatedAuthorHong, Sung Pil-
dc.contributor.affiliatedAuthorKim, Won Ho-
dc.citation.volume22-
dc.citation.number4-
dc.citation.startPage796-
dc.citation.endPage806-
dc.identifier.bibliographicCitationINFLAMMATORY BOWEL DISEASES, Vol.22(4) : 796-806, 2016-
dc.date.modified2017-10-24-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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