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• W1799558752 abstract "Abstract Recent studies have shown that dendritic cells (DCs) regulate B cell functions. In this study, we report that bone marrow (BM)-derived immature DCs, but not mature DCs, can inhibit BCR-induced proliferation of B cells in a contact-dependent manner. This inhibition is overcome by treatment with BAFF and is dependent on the BCR coreceptor CD22; however, it is not dependent on expression of the CD22 glycan ligand(s) produced by ST6Gal-I sialyltransferase. We found that a second CD22 ligand (CD22L) is expressed on CD11c+ splenic and BM-derived DCs, which does not contain ST6Gal-I-generated sialic acids and which, unlike the B cell-associated CD22L, is resistant to neuraminidase treatment and sodium metaperiodate oxidation. Examination of splenic and BM B cell subsets in CD22 and ST6Gal-I knockout mice revealed that ST6Gal-I-generated B cell CD22L plays a role in splenic B cell development, whereas the maintenance of long-lived mature BM B cells depends only on CD22 and not on α2,6-sialic acids produced by ST6Gal-I. We propose that the two distinct CD22L have different functions. The α2,6-sialic acid-containing glycoprotein is important for splenic B cell subset development, whereas the DC-associated ST6Gal-I-independent CD22L may be required for the maintenance of long-lived mature B cells in the BM." @default.
• W1799558752 created "2016-06-24" @default.
• W1799558752 creator A5004809714 @default.
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• W1799558752 creator A5017196291 @default.
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• W1799558752 date "2008-04-01" @default.
• W1799558752 modified "2023-09-26" @default.
• W1799558752 title "Dendritic Cell-Dependent Inhibition of B Cell Proliferation Requires CD22" @default.
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• W1799558752 doi "https://doi.org/10.4049/jimmunol.180.7.4561" @default.
• W1799558752 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2728079" @default.
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• W1799558752 hasPublicationYear "2008" @default.
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