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CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice
dc.creator | Samardžić, T. | |
dc.creator | Gerlach, J | |
dc.creator | Muller, K | |
dc.creator | Marinković, Dragan | |
dc.creator | Hess, J | |
dc.creator | Nitschke, L. | |
dc.creator | Wirth, Thomas | |
dc.date.accessioned | 2021-06-09T13:11:51Z | |
dc.date.available | 2021-06-09T13:11:51Z | |
dc.date.issued | 2002 | |
dc.identifier.issn | 0014-2980 | |
dc.identifier.uri | http://rfasper.fasper.bg.ac.rs/handle/123456789/29 | |
dc.description.abstract | BOB.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.publisher | Wiley-V C H Verlag Gmbh, Weinheim | |
dc.rights | openAccess | |
dc.source | European Journal of Immunology | |
dc.subject | B lymphocyte | en |
dc.subject | cell surface molecule | en |
dc.subject | transcription factor | en |
dc.subject | cellular differentiation | en |
dc.subject | signal transduction | en |
dc.title | CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice | en |
dc.type | article | |
dc.rights.license | ARR | |
dc.citation.epage | 2489 | |
dc.citation.issue | 9 | |
dc.citation.other | 32(9): 2481-2489 | |
dc.citation.rank | M21 | |
dc.citation.spage | 2481 | |
dc.citation.volume | 32 | |
dc.identifier.doi | 10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C | |
dc.identifier.fulltext | http://rfasper.fasper.bg.ac.rs/bitstream/id/362/26.pdf | |
dc.identifier.pmid | 12207332 | |
dc.identifier.scopus | 2-s2.0-0036737191 | |
dc.identifier.wos | 000178144900011 | |
dc.type.version | publishedVersion |