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dc.creatorSamardžić, T.
dc.creatorMarinković, Dragan
dc.creatorDanzer, CP
dc.creatorGerlach, J
dc.creatorNitschke, L.
dc.creatorWirth, Thomas
dc.date.accessioned2021-06-09T13:11:55Z
dc.date.available2021-06-09T13:11:55Z
dc.date.issued2002
dc.identifier.issn0014-2980
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/30
dc.description.abstractCD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.en
dc.publisherWiley-V C H Verlag Gmbh, Weinheim
dc.rightsopenAccess
dc.sourceEuropean Journal of Immunology
dc.subjectmarginal zone B cellen
dc.subjectCD22en
dc.subjectchemokineen
dc.subjectB cell differentiationen
dc.titleReduction of marginal zone B cells in CD22-deficient miceen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage567
dc.citation.issue2
dc.citation.other32(2): 561-567
dc.citation.rankM21
dc.citation.spage561
dc.citation.volume32
dc.identifier.doi10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/367/27.pdf
dc.identifier.pmid11828373
dc.identifier.scopus2-s2.0-0036180761
dc.identifier.wos000173996100029
dc.type.versionpublishedVersion


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