Polymorphism in the Upstream Regulatory Region of the HLA-DQB1 gene in liver graft Recipients.(Statistical Data Included): An article from: Human Biology
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Publisher
Wayne State University Press
ISBN / ASIN
B0008IMCTG
ISBN-13
978B0008IMCT8
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This digital document is an article from Human Biology, published by Wayne State University Press on December 1, 2001. The length of the article is 4602 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.
From the author: Abstract HL4-DQB1*0302 allele frequency is increased in liver graft recipients with acute rejection. We investigated polymorphism in the upstream regulatory regions (URRs) of the DQB1 gene to determine whether polymorphism in the DQB1 promoter region influences liver graft acceptance. A combination of typing protocols based on the polymerase chain reaction were used in 103 first-time liver transplants and 108 healthy Spanish controls. The QBP3.21 allele frequency and QBP3.21-DQBI*0302 haplotype were significantly different in recipients with acute rejection compared to those with good graft acceptance and to controls. Of major interest for acute rejection development are the promoter "splits" of DQB1*0302 (QBP3.21, QBP3.22, and QBP3.3 alleles), which are in linkage disequilibrium with DQBI*0302. The promoter splits were equally distributed in all groups. Thus, although there are significant differences in the frequencies of the QBP alleles and QBP-DQB1 haplotypes between recipients with and without acute reje ction and controls, the composition of these haplotypes is essentially the same in all groups. In conclusion, our data show that the polymorphism in the DQB1 promoter region does not clearly influence liver graft acceptance, and, as occurs in other populations, QBP alleles exhibit strong linkage disequilibrium with the DQB1 locus.
Citation Details
Title: Polymorphism in the Upstream Regulatory Region of the HLA-DQB1 gene in liver graft Recipients.(Statistical Data Included)
Author: M. Muro
Publication:Human Biology (Refereed)
Date: December 1, 2001
Publisher: Wayne State University Press
Volume: 73 Issue: 6 Page: 845(10)
Article Type: Statistical Data Included
Distributed by Thomson Gale
From the author: Abstract HL4-DQB1*0302 allele frequency is increased in liver graft recipients with acute rejection. We investigated polymorphism in the upstream regulatory regions (URRs) of the DQB1 gene to determine whether polymorphism in the DQB1 promoter region influences liver graft acceptance. A combination of typing protocols based on the polymerase chain reaction were used in 103 first-time liver transplants and 108 healthy Spanish controls. The QBP3.21 allele frequency and QBP3.21-DQBI*0302 haplotype were significantly different in recipients with acute rejection compared to those with good graft acceptance and to controls. Of major interest for acute rejection development are the promoter "splits" of DQB1*0302 (QBP3.21, QBP3.22, and QBP3.3 alleles), which are in linkage disequilibrium with DQBI*0302. The promoter splits were equally distributed in all groups. Thus, although there are significant differences in the frequencies of the QBP alleles and QBP-DQB1 haplotypes between recipients with and without acute reje ction and controls, the composition of these haplotypes is essentially the same in all groups. In conclusion, our data show that the polymorphism in the DQB1 promoter region does not clearly influence liver graft acceptance, and, as occurs in other populations, QBP alleles exhibit strong linkage disequilibrium with the DQB1 locus.
Citation Details
Title: Polymorphism in the Upstream Regulatory Region of the HLA-DQB1 gene in liver graft Recipients.(Statistical Data Included)
Author: M. Muro
Publication:Human Biology (Refereed)
Date: December 1, 2001
Publisher: Wayne State University Press
Volume: 73 Issue: 6 Page: 845(10)
Article Type: Statistical Data Included
Distributed by Thomson Gale
