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

Nitschke, Lars; Floyd, Helen; Ferguson, David J.P.; Crocker, Paul R.

doi:10.1084/jem.189.9.1513

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Brief Definitive Report| May 03 1999

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

Lars Nitschke,

Lars Nitschke

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

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Helen Floyd,

Helen Floyd

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

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David J.P. Ferguson,

David J.P. Ferguson

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

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Paul R. Crocker

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

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Author and Article Information

Lars Nitschke

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

Helen Floyd

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

David J.P. Ferguson

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

Paul R. Crocker

From the *Institute for Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany; the ‡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

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: [email protected], 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: [email protected]

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

Received: December 30 1998

Revision Received: February 12 1999

Online ISSN: 1540-9538

Print ISSN: 0022-1007

1999

J Exp Med (1999) 189 (9): 1513–1518.

https://doi.org/10.1084/jem.189.9.1513

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 α2,6-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.

1999

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