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dc.contributor.authorMinamino, Kentoja
dc.contributor.authorTakahara, Kazuhikoja
dc.contributor.authorAdachi, Takumija
dc.contributor.authorNagaoka, Kojija
dc.contributor.authorIyoda, Tomonorija
dc.contributor.authorTaki, Shinsukeja
dc.contributor.authorInaba, Kayoja
dc.contributor.alternative稲葉, カヨja
dc.date.accessioned2013-07-19T06:20:42Z-
dc.date.available2013-07-19T06:20:42Z-
dc.date.issued2012-07-05ja
dc.identifier.issn1460-2377ja
dc.identifier.urihttp://hdl.handle.net/2433/176343-
dc.description.abstractInterferon regulatory factor (IRF)-2 is a transcription factor involved in type I (IFN- α/β) signaling. It has been reported that IRF-2 deficiency results in various immune dysfunctions. However, the role of IRF-2 in B-cell functions needs to be elucidated. Unlike wild-type (WT) B cells, IRF-2(-/-) B2 cells were refractory to anti-IgM, but not LPS. Such a defect in proliferation was dependent on IFN- α/β receptor (IFNAR). Marginal zone B cells increased in the proportion relative to B2 cells in IRF-2(-/-) mice produced IgM normally to LPS stimulation. However, IRF-2(-/-) B2 cells were defective in IgM production in an IFNAR-independent manner, although both B-cell subsets differentiated phenotypically to plasma cells at elevated efficiencies. Class switch recombination of IRF-2(-/-) B2 cells by LPS plus IL-4 was also impaired. Their reduced IgM production was conceivably due to an inefficient up-regulation of Blimp-1. Consistent with these in vitro observations, specific antibody production in vivo to a T-dependent antigen by B2 cells was severely impaired in IRF-2(-/- )mice. However, a low, but significant, level of IgG was detected at a late time point, and this IgG exhibited comparable binding affinity to that in WT mice. Follicular helper T-cell development and germinal center formation were normal. A similar tendency was observed when µ chain(-/-) mice were reconstituted with IRF-2(-/- )B cells. These results revealed a multi-faceted role of IRF-2 in the function of B cells, particularly B2 cells, through regulating proliferation in an IFNAR-dependent manner and antibody production via up-regulation of Blimp-1.ja
dc.format.mimetypeapplication/pdfja
dc.language.isoengja
dc.publisherOxford University Pressja
dc.rights© The Author 2012. Published by Oxford University Press.ja
dc.rightsThis is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。ja
dc.subjectactivationja
dc.subjectantibody productionja
dc.subjectB cellsja
dc.subjectdifferentiationja
dc.subjectinterferon regulatory factor-2ja
dc.subject.meshAnimalsja
dc.subject.meshAntibody Formation/geneticsja
dc.subject.meshB-Lymphocytes/immunologyja
dc.subject.meshB-Lymphocytes/transplantationja
dc.subject.meshCell Differentiation/geneticsja
dc.subject.meshCell Proliferationja
dc.subject.meshCells, Culturedja
dc.subject.meshGene Expression Regulationja
dc.subject.meshImmunoglobulin Class Switching/geneticsja
dc.subject.meshImmunoglobulin mu-Chains/geneticsja
dc.subject.meshInterferon Regulatory Factor-2/geneticsja
dc.subject.meshInterferon Regulatory Factor-2/metabolismja
dc.subject.meshLipopolysaccharides/immunologyja
dc.subject.meshMiceja
dc.subject.meshMice, Inbred C57BLja
dc.subject.meshMice, Knockoutja
dc.subject.meshPlasma Cells/immunologyja
dc.subject.meshPlasma Cells/transplantationja
dc.subject.meshReceptor, Interferon alpha-beta/metabolismja
dc.subject.meshT-Lymphocytes, Helper-Inducer/immunologyja
dc.subject.meshTranscription Factors/geneticsja
dc.subject.meshTranscription Factors/metabolismja
dc.titleIRF-2 regulates B-cell proliferation and antibody production through distinct mechanisms.ja
dc.type.niitypeJournal Articleja
dc.identifier.jtitleInternational immunologyja
dc.identifier.volume24ja
dc.identifier.issue9ja
dc.identifier.spage573ja
dc.identifier.epage581ja
dc.relation.doi10.1093/intimm/dxs060ja
dc.textversionauthorja
dc.identifier.pmid22773153ja
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