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Dendritic Cell-Dependent Inhibition of B Cell Proliferation Requires CD22¹

Lorna Santos^*, Kevin E. Draves, Mark Boton, Prabhjit K. Grewal, Jamey D. Marth and Edward A. Clark^2,*,

^* Department of Immunology and Department of Microbiology, University of Washington, Seattle, WA 98195; and Department of Cellular and Molecular Medicine, Howard Hughes Medical Institute, University of California, La Jolla, CA 92093

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 2,6-sialic acids produced by ST6Gal-I. We propose that the two distinct CD22L have different functions. The 2,6-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.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI55203 and DE16381 (to E.A.C.) and P01HL57345 and the Howard Hughes Medical Institute (to J.D.M.).

² Address correspondence and reprint requests to Dr. Edward A. Clark, Department of Microbiology, Box 357242, University of Washington, 1959 Northeast Pacific Street, Seattle, WA 98195. E-mail address: eclark{at}bart.rprc.washington.edu

³ Abbreviations used in this paper: DC, dendritic cell; LN, lymph node; BM, bone marrow; Au, Arthrobacter ureafaciens; CD22L, CD22 ligand; FO, follicular; iDC, immature DC; mDC, mature DC; MZ, marginal zone; SNA, Sambucus nigra lectin; T1/2, transitional 1/2; FOP, follicular precursor; MZP, MZ precursor; WT, wild type; KO, knockout.

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