| http://purl.uniprot.org/citations/15467837 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15467837 | http://www.w3.org/2000/01/rdf-schema#comment | "The development of autoimmune diabetes in the nonobese diabetic (NOD) mouse results from a breakdown in tolerance to pancreatic islet antigens. CD28-B7 and CD40 ligand-CD40 (CD40L-CD40) costimulatory pathways affect the development of disease and are promising therapeutic targets. Indeed, it was shown previously that diabetes fails to develop in NOD-B7-2-/- and NOD-CD40L-/-mice. In this study, we examined the relative role of these 2 costimulatory pathways in the balance of autoimmunity versus regulation in NOD mice. We demonstrate that initiation but not effector function of autoreactive T cells was defective in NOD-B7-2-/-mice. Moreover, the residual proliferation of the autoreactive cells was effectively controlled by CD28-dependent CD4+CD25+ regulatory T cells (Treg's), as depletion of Treg's partially restored proliferation of autoreactive T cells and resulted in diabetes in an adoptive-transfer model. Similarly, disruption of the CD28-B7 pathway and subsequent Treg deletion restored autoimmunity in NOD-CD40L-/-mice. These results demonstrate that development of diabetes is dependent on a balance of pathogenic and regulatory T cells that is controlled by costimulatory signals. Thus, elimination of Treg's results in diabetes even in the absence of costimulation, which suggests a need for alternative strategies for immunotherapeutic approaches."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci20483"xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Bluestone J.A."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Thompson H.L."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Bour-Jordan H."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Szot G.L."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Bernhard M.R."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/author | "Salomon B.L."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/name | "J Clin Invest"xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/pages | "979-987"xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/title | "Costimulation controls diabetes by altering the balance of pathogenic and regulatory T cells."xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://purl.uniprot.org/core/volume | "114"xsd:string |
| http://purl.uniprot.org/citations/15467837 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15467837 |
| http://purl.uniprot.org/citations/15467837 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15467837 |
| http://purl.uniprot.org/uniprot/#_A0A0X9RAD7-mappedCitation-15467837 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15467837 |
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| http://purl.uniprot.org/uniprot/#_Q0VEI3-mappedCitation-15467837 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15467837 |
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