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dc.creatorAmano, H.
dc.creatorAmano, E.
dc.creatorMoll, T.
dc.creatorMarinković, Dragan
dc.creatorIbnou-Zekri, N
dc.creatorMartinez-Soria, E.
dc.creatorSemac, I
dc.creatorWirth, Thomas
dc.creatorNitschke, L.
dc.creatorIzui, S
dc.date.accessioned2021-06-09T13:12:04Z
dc.date.available2021-06-09T13:12:04Z
dc.date.issued2003
dc.identifier.issn0022-1767
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/32
dc.description.abstractThe accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.en
dc.publisherAmer Assoc Immunologists, Bethesda
dc.rightsopenAccess
dc.sourceJournal of Immunology
dc.titleThe Yaa mutation promoting murine lupus causes defective development of marginal zone B cellsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage2301
dc.citation.issue5
dc.citation.other170(5): 2293-2301
dc.citation.rankaM21
dc.citation.spage2293
dc.citation.volume170
dc.identifier.doi10.4049/jimmunol.170.5.2293
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/385/29.pdf
dc.identifier.pmid12594250
dc.identifier.scopus2-s2.0-0037371122
dc.identifier.wos000181146800007
dc.type.versionpublishedVersion


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