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IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5.

Shin, JH ; Janer, M ; McNeney, B ; Blay, S ; Deutsch, K ; Sanjeevi, CB ; Kockum, I ; Lernmark, Åke LU orcid ; Graham, J and Diabetes Incidence in Sweden Study Group, The , et al. (2007) In Genes Immun. 8(6). p.503-512
Abstract
In a large case-control study of Swedish incident type I diabetes patients and controls, 0–34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2... (More)
In a large case-control study of Swedish incident type I diabetes patients and controls, 0–34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 times 10-13) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 times 10-5) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
polyadenylation signal, IA-2 autoantibodies, GIMAP5, type I diabetes
in
Genes Immun.
volume
8
issue
6
pages
503 - 512
external identifiers
  • scopus:34548499874
  • pmid:17641683
DOI
10.1038/sj.gene.6364413
language
English
LU publication?
yes
id
bad435fe-dffe-4447-b4e0-e358ddc329e7 (old id 1140902)
date added to LUP
2016-04-04 14:15:06
date last changed
2022-02-14 01:05:59
@article{bad435fe-dffe-4447-b4e0-e358ddc329e7,
  abstract     = {{In a large case-control study of Swedish incident type I diabetes patients and controls, 0–34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 times 10-13) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 times 10-5) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease.}},
  author       = {{Shin, JH and Janer, M and McNeney, B and Blay, S and Deutsch, K and Sanjeevi, CB and Kockum, I and Lernmark, Åke and Graham, J and Diabetes Incidence in Sweden Study Group, The and Swedish Childhood Diabetes Study Group, The}},
  keywords     = {{polyadenylation signal; IA-2 autoantibodies; GIMAP5; type I diabetes}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{503--512}},
  series       = {{Genes Immun.}},
  title        = {{IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5.}},
  url          = {{http://dx.doi.org/10.1038/sj.gene.6364413}},
  doi          = {{10.1038/sj.gene.6364413}},
  volume       = {{8}},
  year         = {{2007}},
}