Приказ основних података о документу

dc.creatorSamardžić, T.
dc.creatorGerlach, J
dc.creatorMuller, K
dc.creatorMarinković, Dragan
dc.creatorHess, J
dc.creatorNitschke, L.
dc.creatorWirth, Thomas
dc.date.accessioned2021-06-09T13:11:51Z
dc.date.available2021-06-09T13:11:51Z
dc.date.issued2002
dc.identifier.issn0014-2980
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/29
dc.description.abstractBOB.1/OBF1 (also called OCA-B), a B lymphocyte-specific transcriptional coactivator, is recruited to octamer-containing promoters by interacting with the Oct-1 or Oct-2 proteins. BOB.1/OBF.1-deficient mice show impaired secondary immunoglobulin isotype secretion and complete absence of germinal centers. Furthermore, numbers of splenic B cells are reduced due to a developmental block at the transitional B cell stage in the bone marrow. We found that surface expression of CD22 is selectively increased on B lineage cells in the bone marrow of BOB.1/OBF.1-deficient mice. CD22 is known as a negative regulator of B cell receptor signaling. We therefore investigated whether defects in B cell development in the BOB.1/OBF1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1 xCD22 double-deficient mice, numbers of transitional B cells in the bone marrow were normal. Consequently, double-deficient mice also had normal B to T cell ratios in the spleen. We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca2+ mobilization. This Ca2+-signalling defect was restored in BOBA/ OBF1 xCD22 double-deficient B cells. Nevertheless, double-deficient animals were unable to mount humoral immune responses and to form germinal centers. Finally, we demonstrate that CD22(-/-) splenic B cells proliferate independently of BOB.1/OBF1 upon stimulation with LPS. These studies suggest that the B cell differentiation defect observed in BOB.1/OBF.1(-/-) mice is BCR-signal dependent. However, the impairment in germinal center formation is caused by a different mechanism.en
dc.publisherWiley-V C H Verlag Gmbh, Weinheim
dc.rightsopenAccess
dc.sourceEuropean Journal of Immunology
dc.subjectB lymphocyteen
dc.subjectcell surface moleculeen
dc.subjecttranscription factoren
dc.subjectcellular differentiationen
dc.subjectsignal transductionen
dc.titleCD22 regulates early B cell development in BOB.1/OBF.1-deficient miceen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage2489
dc.citation.issue9
dc.citation.other32(9): 2481-2489
dc.citation.rankM21
dc.citation.spage2481
dc.citation.volume32
dc.identifier.doi10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/362/26.pdf
dc.identifier.pmid12207332
dc.identifier.scopus2-s2.0-0036737191
dc.identifier.wos000178144900011
dc.type.versionpublishedVersion


Документи

Thumbnail

Овај документ се појављује у следећим колекцијама

Приказ основних података о документу