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dc.contributor.authorBhattacharyya, Sen
dc.contributor.authorDeb, Jen
dc.contributor.authorPatra, AKen
dc.contributor.authorThuy Pham, DAen
dc.contributor.authorChen, Wen
dc.contributor.authorVaeth, Men
dc.contributor.authorBerberich-Siebelt, Fen
dc.contributor.authorKlein-Hessling, Sen
dc.contributor.authorLamperti, EDen
dc.contributor.authorReifenberg, Ken
dc.contributor.authorJellusova, Jen
dc.contributor.authorSchweizer, Aen
dc.contributor.authorNitschke, Len
dc.contributor.authorLeich, Een
dc.contributor.authorRosenwald, Aen
dc.contributor.authorBrunner, Cen
dc.contributor.authorEngelmann, Sen
dc.contributor.authorBommhardt, Uen
dc.contributor.authorAvots, Aen
dc.contributor.authorMüller, MRen
dc.contributor.authorKondo, Een
dc.contributor.authorSerfling, Een
dc.date.accessioned2018-05-14T13:10:22Z
dc.date.available2018-05-14T13:10:22Z
dc.date.issued2011-04-11en
dc.identifier.urihttp://hdl.handle.net/10026.1/11503
dc.description.abstract

By studying mice in which the Nfatc1 gene was inactivated in bone marrow, spleen, or germinal center B cells, we show that NFATc1 supports the proliferation and suppresses the activation-induced cell death of splenic B cells upon B cell receptor (BCR) stimulation. BCR triggering leads to expression of NFATc1/αA, a short isoform of NFATc1, in splenic B cells. NFATc1 ablation impaired Ig class switch to IgG3 induced by T cell-independent type II antigens, as well as IgG3(+) plasmablast formation. Mice bearing NFATc1(-/-) B cells harbor twofold more interleukin 10-producing B cells. NFATc1(-/-) B cells suppress the synthesis of interferon-γ by T cells in vitro, and these mice exhibit a mild clinical course of experimental autoimmune encephalomyelitis. In large part, the defective functions of NFATc1(-/-) B cells are caused by decreased BCR-induced Ca(2+) flux and calcineurin (Cn) activation. By affecting CD22, Rcan1, CnA, and NFATc1/αA expression, NFATc1 controls the Ca(2+)-dependent Cn-NFAT signaling network and, thereby, the fate of splenic B cells upon BCR stimulation.

en
dc.format.extent823 - 839en
dc.languageengen
dc.language.isoengen
dc.subjectAnimalsen
dc.subjectB-Lymphocytesen
dc.subjectCalcineurinen
dc.subjectCalciumen
dc.subjectImmunoglobulin Class Switchingen
dc.subjectLymphocyte Activationen
dc.subjectMiceen
dc.subjectNFATC Transcription Factorsen
dc.subjectReceptors, Antigen, B-Cellen
dc.subjectSignal Transductionen
dc.subjectSpleenen
dc.subjectT-Lymphocytesen
dc.titleNFATc1 affects mouse splenic B cell function by controlling the calcineurin--NFAT signaling network.en
dc.typeJournal Article
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/21464221en
plymouth.issue4en
plymouth.volume208en
plymouth.publication-statusPublisheden
plymouth.journalJ Exp Meden
dc.identifier.doi10.1084/jem.20100945en
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeUnited Statesen
dc.identifier.eissn1540-9538en
dc.rights.embargoperiodNo embargoen
rioxxterms.versionofrecord10.1084/jem.20100945en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.typeJournal Article/Reviewen


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