| http://purl.uniprot.org/citations/23904159 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23904159 | http://www.w3.org/2000/01/rdf-schema#comment | "Self-reactive B cells in BALB/c AM14 transgenic (Tg) rheumatoid factor mice are not subject to central or peripheral tolerization. Instead, they remain at a stage of "clonal ignorance"; that is, they do not proliferate and differentiate into Ab-forming cells. However, the immunoregulatory mechanisms that prevent autoantibody production in these mice remain unclear. In this study, we show that crossing AM14 Tg mice to a mouse strain deficient in Act1, a molecule involved in the regulation of BAFF-R and CD40-signaling in B cells, results in spontaneous activation of AM14 Tg B cells and production of AM14-specific Abs. Three-to 5-mo-old AM14 Tg Act1(-/-) mice showed significant expansion of AM14 Tg B cells, including a 2-to 3-fold increase in the spleen and cervical lymph nodes compared with AM14 Tg Act1(+/+) mice. Furthermore, in the presence of endogenous self-Ag (IgH(a) congenic background), AM14 Tg Act1(-/-) B cells were spontaneously activated and differentiated into Ab-forming cells. In contrast with previous studies using AM14 Tg MLR.Fas(lpr) mice, we found that a significant number of AM14 Tg cells AM14 Tg Act1(-/-) mice displayed phenotypic characteristics of germinal center B cells. Anti-CD40L treatment significantly limited the expansion and activation of AM14 Tg Act1(-/-) B cells, suggesting that CD40L-mediated signals are required for the retention of these cells. Our results support the important role of Act1 in the regulation of self-reactive B cells and reveal how Act1 functions to prevent the production of autoantibodies."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1300152"xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Lu Y."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Li X."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Shlomchik M.J."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Giltiay N.V."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Jorgensen T.N."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/author | "Cullen J.L."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/pages | "2155-2163"xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/title | "Spontaneous loss of tolerance of autoreactive B cells in Act1-deficient rheumatoid factor transgenic mice."xsd:string |
| http://purl.uniprot.org/citations/23904159 | http://purl.uniprot.org/core/volume | "191"xsd:string |
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