Journal of Biological Chemistry
Volume 275, Issue 48, 1 December 2000, Pages 37984-37992
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MOLECULAR BASIS OF CELL AND DEVELOPMENTAL BIOLOGY
CD47, a Ligand for the Macrophage Fusion Receptor, Participates in Macrophage Multinucleation*

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The macrophage fusion receptor (MFR), also called P84/BIT/SIRPα/SHPS-1, is a transmembrane glycoprotein that belongs to the superfamily of immunoglobulins. Previously, we showed that MFR expression is highly induced at the onset of fusion in macrophages, and that MFR appears to play a role in macrophage-macrophage adhesion/fusion leading to multinucleation. The recent finding that IAP/CD47 acts as a ligand for MFR led us to hypothesize that it interacts with CD47 at the onset of cell-cell fusion. CD47 is a transmembrane glycoprotein, which, like MFR, belongs to the superfamily of immunoglobulins. We show that macrophages express the hemopoietic form of CD47, the expression of which is induced at the onset of fusion, but to a lower level than MFR. A glutathioneS-transferase CD47 fusion protein engineered to contain the extracellular domain of CD47, binds macrophages, associates with MFR, and prevents multinucleation. CD47 and MFR associate via their amino-terminal immunoglobulin variable domain. Of the nine monoclonal antibodies raised against the extracellular domain of CD47, three block fusion, as well as MFR-CD47 interaction, whereas the others have no effect. Together, these data suggest that CD47 is involved in macrophage multinucleation by virtue of interacting with MFR during adhesion/fusion.

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Published, JBC Papers in Press, August 29, 2000, DOI 10.1074/jbc.M002334200

*

This work was supported by National Institutes of Health Grants DE12110 (to A. V.) and GM57573-01 (to F. P. L.) and by a grant from Monsanto to Washington University (to F. P. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

**

These authors made equal contributions to this work.