The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1999/5/1513/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 9, May 3, 1999 1513-1518

Brief Definitive Reports

Identification of CD22 Ligands on Bone Marrow Sinusoidal Endothelium Implicated in CD22-dependent Homing of Recirculating B Cells

Lars Nitschke*, Helen Floyd{ddagger}, David J.P. Ferguson§, and Paul R. Crocker{ddagger}

From the * Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the {ddagger} Department of Biochemistry, University of Dundee, Dundee DD1 5EH, United Kingdom; and the § Electron Microscopy Unit, Nuffield Department of Pathology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom

CD22 is a B cell–specific transmembrane protein known to function as a negative regulator of B cell signaling. It has also been implicated in cell adhesion through recognition of {alpha}2,6-linked sialic acids on glycans of target cells. Previous studies showed that CD22-deficient mice had a strongly reduced population of mature recirculating B cells in the bone marrow despite normal B cell development. Using a soluble recombinant form of the receptor (CD22-Fc), we demonstrate here that sialylated ligands for CD22 are expressed on sinusoidal endothelial cells of murine bone marrow but not on endothelial cells in other tissues examined. Injection of CD22-Fc revealed that the CD22 ligands in the bone marrow were accessible to the circulation. Treatment of mice with either CD22-Fc or affinity-purified anti-CD22 antibody led to an ~50% reduction in mature recirculating B cells in the bone marrow without affecting numbers in the spleen. Finally, consistent with the notion that CD22 is a homing receptor, we show that compared with wild-type mice, CD22-deficient animals have a lower number of immunoglobulin M–secreting plasma cells in the bone marrow.

Key Words: lymphocyte homing • B cells • sialic acid binding • siglec • CD22

Address correspondence to Lars Nitschke, Institute for Virology and Immunobiology, University of Würzburg, Versbacherstr. 7, 97078 Würzburg, Germany. Phone: 49-931-201-3957; Fax: 49-931-201-2243; E-mail: nitschke{at}vim.uni-wuerzburg.de, or to Paul R. Crocker, Department of Biochemistry, University of Dundee, Dundee DD1 5EH, UK. Phone: 44-1382-345781; Fax: 44-1382-345855; E-mail: prcrocker{at}bad.dundee.ac.uk

L. Nitschke and H. Floyd contributed equally to this work.


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