| http://purl.uniprot.org/citations/19152335 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19152335 | http://www.w3.org/2000/01/rdf-schema#comment | "Systemic lupus erythematosus pathology reflects autoantibody-mediated damage due to a failure of B-lymphocyte tolerance. We previously reported that B-lymphopenic A/WySnJ mice develop a lupus-like syndrome and linked this syndrome to the B-cell maturation defect-1 (Bcmd-1) mutant allele of the B-cell-activating factor belonging to the TNF family-receptor (Baffr) gene. Here, we further evaluate the genetic basis for autoimmunity in A/WySnJ mice. We produced B6.Bcmd-1 and AW.Baffr(-/-) congenic mice (N5), and compared them with B6.Baffr(-/-) and A/WySnJ mice with respect to B-lymphocyte development. Bcmd-1-expressing mice had more B cells with greater maturity than Baffr(-/-) mice regardless of genetic background, indicating that Bcmd-1 encodes a partially functional BAFF-R. We also compared these mice for lupus phenotypes to determine whether Bcmd-1 is necessary and sufficient for disease, or whether the Baffr(-/-) (-) allele can also cause autoimmunity. The Baffr(-/-) allele did not lead to autoimmunity on either genetic background. In contrast, the Bcmd-1 allele was necessary and sufficient for development of low levels of IgM autoantibodies in B6.Bcmd-1 mice. However, Bcmd-1 plus unidentified A/WySnJ modifier genes were necessary for development of IgG autoantibodies and renal pathology. We propose that in A/WySnJ mice an excess of BAFF per B cell rescues self-reactive B cells through a partially functional BAFF-R in a B-lymphopenic environment."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.org/dc/terms/identifier | "doi:10.1002/eji.200838569"xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/author | "Sasaki Y."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/author | "Hayes C.E."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/author | "Nashold F.E."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/author | "Mayne C.G."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/name | "Eur J Immunol"xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/pages | "589-599"xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/title | "Altered BAFF-receptor signaling and additional modifier loci contribute to systemic autoimmunity in A/WySnJ mice."xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://purl.uniprot.org/core/volume | "39"xsd:string |
| http://purl.uniprot.org/citations/19152335 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19152335 |
| http://purl.uniprot.org/citations/19152335 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19152335 |
| http://purl.uniprot.org/uniprot/#_A0A0U5J6R6-mappedCitation-19152335 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19152335 |
| http://purl.uniprot.org/uniprot/#_A0A2R8VI78-mappedCitation-19152335 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19152335 |
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| http://purl.uniprot.org/uniprot/#_Q3KP92-mappedCitation-19152335 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19152335 |
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| http://purl.uniprot.org/uniprot/#_Q8BZM8-mappedCitation-19152335 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19152335 |