| http://purl.uniprot.org/citations/20513733 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20513733 | http://www.w3.org/2000/01/rdf-schema#comment | "Peripheral B-cell numbers are tightly regulated by homeostatic mechanisms that influence the transitional and mature B-cell compartments and dictate the size and clonotypic diversity of the B-cell repertoire. B-lymphocyte stimulator (BLyS, a trademark of Human Genome Sciences, Inc.) plays a key role in regulating peripheral B-cell homeostasis. CD22 also promotes peripheral B-cell survival through ligand-dependent mechanisms. The B-cell subsets affected by the absence of BLyS and CD22 signals overlap, suggesting that BLyS- and CD22-mediated survival are intertwined. To examine this, the effects of BLyS insufficiency following neutralizing BLyS mAb treatment in mice also treated with CD22 ligand-blocking mAb were examined. Combined targeting of the BLyS and CD22 survival pathways led to significantly greater clearance of recirculating bone marrow, blood, marginal zone and follicular B cells than either treatment alone. Likewise, BLyS blockade further reduced bone marrow, blood and spleen B-cell numbers in CD22(-/-) mice. Notably, BLyS receptor expression and downstream signaling were normal in CD22(-/-) B cells, suggesting that CD22 does not directly alter BLyS responsiveness. CD22 survival signals were likewise intact in the absence of BLyS, as CD22 mAb treatment depleted blood B cells from mice with impaired BLyS receptor 3 (BR3) signaling. Finally, enforced BclxL expression, which rescues BR3 impairment, did not affect B-cell depletion following CD22 mAb treatment. Thus, the current studies support a model whereby CD22 and BLyS promote the survival of overlapping B-cell subsets but contribute to their maintenance through independent and complementary signaling pathways."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.org/dc/terms/identifier | "doi:10.1093/intimm/dxq055"xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Haas K.M."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Tedder T.F."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Ward C.D."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Poe J.C."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Migone T.S."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Smith S.H."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/author | "Yanaba K."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/name | "Int Immunol"xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/pages | "681-691"xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/title | "B-cell homeostasis requires complementary CD22 and BLyS/BR3 survival signals."xsd:string |
| http://purl.uniprot.org/citations/20513733 | http://purl.uniprot.org/core/volume | "22"xsd:string |
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