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dc.creatorSamardžić, T.
dc.creatorMarinković, Dragan
dc.creatorNielsen, P.J.
dc.creatorNitschke, L.
dc.creatorWirth, Thomas
dc.date.accessioned2021-06-09T13:11:48Z
dc.date.available2021-06-09T13:11:48Z
dc.date.issued2002
dc.identifier.issn0270-7306
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/28
dc.description.abstractMarginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type It T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack. of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice.en
dc.publisherAmer Soc Microbiology, Washington
dc.rightsopenAccess
dc.sourceMolecular and Cellular Biology
dc.titleBOB.1OBF.1 deficiency affects marginal-zone B-cell compartmenten
dc.typearticle
dc.rights.licenseARR
dc.citation.epage8331
dc.citation.issue23
dc.citation.other22(23): 8320-8331
dc.citation.rankaM21
dc.citation.spage8320
dc.citation.volume22
dc.identifier.doi10.1128/MCB.22.23.8320-8331.2002
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/357/25.pdf
dc.identifier.pmid12417733
dc.identifier.scopus2-s2.0-0036889190
dc.identifier.wos000179190600020
dc.type.versionpublishedVersion


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