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http://purl.uniprot.org/citations/19895409http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Background

Established genetic susceptibility loci for type 1 diabetes are important in immune regulation and may play a role also in atopic disorders, potentially explaining the inverse association between childhood eczema and subsequent risk for type 1 diabetes previously reported.

Objective

We aimed to directly assess whether HLA-DQ, CTLA4, and PTPN22 genes could explain the putative association between childhood eczema and lower subsequent risk of type 1 diabetes observed in several case-control studies.

Methods

We designed a case-control study with 339 incident cases of type 1 diabetes identified in the Norwegian childhood diabetes registry, and 985 population-based control children. DNA was collected, and physician-diagnosed childhood eczema was ascertained by a questionnaire administered to the parents of children with and without type 1 diabetes.

Results

The previously reported association between childhood eczema and lower risk of type 1 diabetes was confirmed (odds ratio,OR, 0.61, 95% confidence interval, CI, 0.40-0.95] and this was consistent in subgroups defined by HLA-DQ, CTLA4, and PTPN22 genotypes. The OR was essentially not influenced by adjustment for genetic variation at these loci (OR simultaneously adjusted for the three genetic loci: 0.55, 95% CI: 0.32-0.92). The ratio of the unadjusted to adjusted OR was 1.12, with a corresponding 95% CI from 0.84 to 1.50.

Conclusion

In this first study of its kind, we demonstrated directly that the observed inverse association between childhood eczema and type 1 diabetes is not likely to be explained by the established diabetes susceptibility genes HLA-DQ, CTLA4, or PTPN22."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.org/dc/terms/identifier"doi:10.1111/j.1399-5448.2009.00605.x"xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/author"Undlien D.E."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/author"Ronningen K.S."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/author"Joner G."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/author"Stene L.C."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/author"Bjornvold M."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/name"Pediatr Diabetes"xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/pages"386-393"xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/title"An inverse association between history of childhood eczema and subsequent risk of type 1 diabetes that is not likely to be explained by HLA-DQ, PTPN22, or CTLA4 polymorphisms."xsd:string
http://purl.uniprot.org/citations/19895409http://purl.uniprot.org/core/volume"11"xsd:string
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