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dc.contributor.authorBhattacharyya, S
dc.contributor.authorDeb, J
dc.contributor.authorPatra, AK
dc.contributor.authorThuy Pham, DA
dc.contributor.authorChen, W
dc.contributor.authorVaeth, M
dc.contributor.authorBerberich-Siebelt, F
dc.contributor.authorKlein-Hessling, S
dc.contributor.authorLamperti, ED
dc.contributor.authorReifenberg, K
dc.contributor.authorJellusova, J
dc.contributor.authorSchweizer, A
dc.contributor.authorNitschke, L
dc.contributor.authorLeich, E
dc.contributor.authorRosenwald, A
dc.contributor.authorBrunner, C
dc.contributor.authorEngelmann, S
dc.contributor.authorBommhardt, U
dc.contributor.authorAvots, A
dc.contributor.authorMüller, MR
dc.contributor.authorKondo, E
dc.contributor.authorSerfling, E
dc.date.accessioned2018-05-14T13:10:22Z
dc.date.available2018-05-14T13:10:22Z
dc.date.issued2011-04-11
dc.identifier.issn0022-1007
dc.identifier.issn1540-9538
dc.identifier.urihttp://hdl.handle.net/10026.1/11503
dc.description.abstract

<jats:p>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 Ca2+ flux and calcineurin (Cn) activation. By affecting CD22, Rcan1, CnA, and NFATc1/αA expression, NFATc1 controls the Ca2+-dependent Cn–NFAT signaling network and, thereby, the fate of splenic B cells upon BCR stimulation.</jats:p>

dc.format.extent823-839
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherRockefeller University Press
dc.subjectAnimals
dc.subjectB-Lymphocytes
dc.subjectCalcineurin
dc.subjectCalcium
dc.subjectImmunoglobulin Class Switching
dc.subjectLymphocyte Activation
dc.subjectMice
dc.subjectNFATC Transcription Factors
dc.subjectReceptors, Antigen, B-Cell
dc.subjectSignal Transduction
dc.subjectSpleen
dc.subjectT-Lymphocytes
dc.titleNFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/21464221
plymouth.issue4
plymouth.volume208
plymouth.publisher-urlhttp://dx.doi.org/10.1084/jem.20100945
plymouth.publication-statusPublished
plymouth.journalJournal of Experimental Medicine
dc.identifier.doi10.1084/jem.20100945
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 States
dc.identifier.eissn1540-9538
dc.rights.embargoperiodNo embargo
rioxxterms.versionofrecord10.1084/jem.20100945
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review


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