http://purl.uniprot.org/citations/18984740 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18984740 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectiveEfforts to map non-major histocompatibility complex (MHC) genes causing type 1 diabetes in NOD mice identified Slc11a1, formerly Nramp1, as the leading candidate gene in the Idd5.2 region. Slc11a1 is a membrane transporter of bivalent cations that is expressed in late endosomes and lysosomes of macrophages and dendritic cells (DCs). Because DCs are antigen-presenting cells (APCs) known to be critically involved in the immunopathogenic events leading to type 1 diabetes, we hypothesized that Slc11a1 alters the processing or presentation of islet-derived antigens to T-cells.Research design and methodsNOD mice having wild-type (WT) or mutant Slc11a1 molecules and 129 mice having WT or null Slc11a1 alleles were examined for parameters associated with antigen presentation.ResultsWe found that Slc11a1 enhanced the presentation of a diabetes-related T-cell determinant of GAD65, and its function contributed to the activation of a pathogenic T-cell clone, BDC2.5. An enhanced generation of interferon (IFN)-gamma-producing T-cells was also associated with functional Slc11a1. The alteration of immune responsiveness by Slc11a1 genotype did not correlate with altered MHC class II expression in DCs; however, functional Slc11a1 was associated with accelerated phagocytosis and phagosomal acidification in DCs.ConclusionsThe association of variants encoding Slc11a1 with type 1 diabetes may reflect its function in processing and presentation of islet self-antigens in DCs. Thus, non-MHC genes could affect the MHC-restricted T-cell response through altered antigen processing and presentation."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.org/dc/terms/identifier | "doi:10.2337/db07-1608"xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Gros P."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Wicker L.S."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Sercarz E.E."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Dai Y.D."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Zaghouani H."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/author | "Marrero I.G."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/pages | "156-164"xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/title | "Slc11a1 enhances the autoimmune diabetogenic T-cell response by altering processing and presentation of pancreatic islet antigens."xsd:string |
http://purl.uniprot.org/citations/18984740 | http://purl.uniprot.org/core/volume | "58"xsd:string |
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