| http://purl.uniprot.org/citations/11812739 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11812739 | http://www.w3.org/2000/01/rdf-schema#comment | "For poorly understood reasons, the development of autoimmune diabetes in humans and mice is dominantly inhibited by major histocompatibility complex (MHC) class II molecules with diverse antigen-binding sites. We have previously shown that thymocytes expressing a highly diabetogenic I-A(g7)-restricted T-cell receptor (TCR) (4.1-TCR) undergo negative selection in mice carrying one copy of the antidiabetogenic H-2(b) haplotype in an I-A(b)-dependent but superantigen-independent manner. Here, we show that 4.1-TCR-transgenic thymocytes undergo different forms of tolerance in NOD mice expressing antidiabetogenic I-A(d), I-A(g7PD), or I-Ealpha(k) transgenes. The ability of protective MHC class II molecules to induce thymocyte tolerance in 4.1-TCR-transgenic NOD mice correlates with their ability to prevent diabetes in non-TCR-transgenic mice and is associated with polymorphisms within positions 56-67 of their beta1 domains. The 4.1-thymocyte tolerogenic activity of these MHC class II molecules is mediated by dendritic cells and macrophages but not by B-cells or thymic epithelial cells and is a peptide-dependent process. Antidiabetogenic MHC class II molecules may thus afford diabetes resistance by presenting, on dendritic cells and macrophages, tolerogenic peptides to a subset of highly diabetogenic and MHC-promiscuous CD4(+) T-cells that play a critical role in the initiation of diabetes."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.51.2.325"xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/author | "Santamaria P."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/author | "Amrani A."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/author | "Serra P."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/author | "Verdaguer J."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/author | "Thiessen S."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/pages | "325-338"xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/title | "T-cell tolerance by dendritic cells and macrophages as a mechanism for the major histocompatibility complex-linked resistance to autoimmune diabetes."xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://purl.uniprot.org/core/volume | "51"xsd:string |
| http://purl.uniprot.org/citations/11812739 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11812739 |
| http://purl.uniprot.org/citations/11812739 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11812739 |
| http://purl.uniprot.org/uniprot/#_P01849-mappedCitation-11812739 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/11812739 |
| http://purl.uniprot.org/uniprot/P01849 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/11812739 |