http://purl.uniprot.org/citations/16567828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16567828 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectiveThe overlap between genetic susceptibility to celiac disease (CD) and to type 1 diabetes is incomplete; therefore, some genetic polymorphisms may significantly modify the risk of CD in subjects with type 1 diabetes. This study aimed to investigate whether the susceptibility to CD in diabetic children is modified by positivity for HLA-DQB1*02-DQA1*05 and DQB1*0302-DQA1*03 and by alleles of single nucleotide polymorphisms within the genes encoding CTLA4, transforming growth factor (TGF)-beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1, IL-2, IL-6, and IL-10.Research design and methodsGenotypic data were compared between 130 case subjects (children with type 1 diabetes and CD diagnosed using endomysium antibodies) and 245 control subjects (children with type 1 diabetes only, optimally two per case, matched for center, age at type 1 diabetes onset, and type 1 diabetes duration). The subjects were recruited from 10 major European pediatric diabetes centers performing regular screening for CD. The polymorphisms were determined using PCR with sequence-specific primers, and the risk was assessed by building a step-up conditional logistic regression model using variables that were significantly associated with CD in the univariate analysis.ResultsThe best-fitted model showed that risk of CD is increased by presence of HLA-DQB1*02-DQA1*05 (odds ratio 4.5 [95% CI 1.8-11], for homozygosity, and 2.0 [1.1-3.7], for a single dose) and also independently by TNF -308A (1.9 [1.1-3.2], for phenotypic positivity), whereas IL1-alpha -889T showed a weak negative association (0.6 [0.4-0.9]).ConclusionsThe results indicate that the risk of CD in children with type 1 diabetes is significantly modified both by the presence of HLA-DQB1*02-DQA1*05 and by a variant of another gene within the major histocompatibility complex, the TNF -308A."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.org/dc/terms/identifier | "doi:10.2337/diacare.29.04.06.dc05-1923"xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Battelino T."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Lebl J."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Schober E."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Cinek O."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Sumnik Z."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Kordonouri O."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Kulich M."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Soltesz G."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Arato A."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Bratanic N."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Danne T."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/author | "Roszai B."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/name | "Diabetes Care"xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/pages | "858-863"xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/title | "Risk of celiac disease in children with type 1 diabetes is modified by positivity for HLA-DQB1*02-DQA1*05 and TNF -308A."xsd:string |
http://purl.uniprot.org/citations/16567828 | http://purl.uniprot.org/core/volume | "29"xsd:string |
http://purl.uniprot.org/citations/16567828 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16567828 |
http://purl.uniprot.org/citations/16567828 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16567828 |
http://purl.uniprot.org/uniprot/#_A0A0E3DC97-mappedCitation-16567828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16567828 |
http://purl.uniprot.org/uniprot/#_A0A0E3DC99-mappedCitation-16567828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16567828 |
http://purl.uniprot.org/uniprot/#_A0A076L4M5-mappedCitation-16567828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16567828 |