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http://purl.uniprot.org/citations/15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15240665http://www.w3.org/2000/01/rdf-schema#comment"Although HLA-DQ8 has been implicated as a key determinant of genetic susceptibility to human type 1 diabetes, spontaneous diabetes has been observed in HLA-DQ8 transgenic mice that lack expression of murine MHC class II molecules (mII(-/-)) only when the potent costimulatory molecule, B7.1, is transgenically expressed on pancreatic beta cells. To study the contribution of HLA-DQ8 to the development of diabetes in this model, we crossed RIP-B7.1mII(-/-) mice with a set of transgenic mouse lines that differed in their HLA-DQ8 expression patterns on APC subpopulations, in particular dendritic cells and cortical thymic epithelial cells. Surprisingly, we found that even in the absence of HLA-DQ8 and CD4 T cells, a substantial fraction of the RIP-B7.1mII(-/-) mice developed diabetes. This disease process was remarkable for not only showing insulitis, but also inflammatory destruction of the exocrine pancreas with diffusely up-regulated expression of MHC class I and ICAM-1 molecules. Expression of HLA-DQ8 markedly increased the kinetics and frequency of diabetes, with the most severe disease in the lines with the highest levels of HLA-DQ8 on cortical thymic epithelial cells and the largest numbers of CD4 T cells. However, the adoptive transfer of diabetes was not HLA-DQ8-dependent and disease could be rapidly induced with purified CD8 T cells alone. Expression of B7.1 in the target tissue can thus dramatically alter the cellular and molecular requirements for the development of autoimmunity."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.173.2.787"xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Klein L."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Taylor J.A."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Lennon-Dumenil A.M."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Lipes M.A."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Wucherpfennig K.W."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Neely D."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"McInerney M.F."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/author"Havari E."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/pages"787-796"xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/title"Expression of the B7.1 costimulatory molecule on pancreatic beta cells abrogates the requirement for CD4 T cells in the development of type 1 diabetes."xsd:string
http://purl.uniprot.org/citations/15240665http://purl.uniprot.org/core/volume"173"xsd:string
http://purl.uniprot.org/citations/15240665http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15240665
http://purl.uniprot.org/citations/15240665http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15240665
http://purl.uniprot.org/uniprot/#_A0A1D8M9B3-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_A0A494B9G5-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_A0A494B9U2-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_P06342-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_P06343-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_P06345-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665
http://purl.uniprot.org/uniprot/#_P06346-mappedCitation-15240665http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15240665