2B4 is a cell surface glycoprotein related to CD2 and implicated in the regulation of natural killer and T lymphocyte function. A recombinant protein containing the extracellular region of mouse (m)2B4 attached to avidin-coated fluorescent beads bound to rodent cells, and binding was completely blocked by CD48 monoclonal antibodies (mAbs). Using surface plasmon resonance, we showed that purified soluble mCD48 bound m2B4 with a six- to ninefold higher affinity (Kd ≈ 16 μM at 37°C) than its other ligand, CD2. Human CD48 bound human 2B4 with a similar affinity (Kd ≈ 8 μM). The finding of an additional ligand for CD48 provides an explanation for distinct functional effects observed on perturbing CD2 and CD48 with mAbs or by genetic manipulation.
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7 December 1998
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December 07 1998
2B4, the Natural Killer and T Cell Immunoglobulin Superfamily Surface Protein, Is a Ligand for CD48
Marion H. Brown,
Marion H. Brown
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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Kent Boles,
Kent Boles
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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P. Anton van der Merwe,
P. Anton van der Merwe
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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Vinay Kumar,
Vinay Kumar
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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Porunelloor A. Mathew,
Porunelloor A. Mathew
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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A. Neil Barclay
A. Neil Barclay
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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Marion H. Brown
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Kent Boles
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
P. Anton van der Merwe
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Vinay Kumar
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Porunelloor A. Mathew
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
A. Neil Barclay
From the *Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom; the ‡Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107; and the §Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Address correspondence to Marion H. Brown, MRC Cellular Immunology Unit, Sir William Dunn School of Pathology, South Parks Rd., Oxford, OX1 3RE, UK. Phone: 01-865-275-594; Fax: 01-865-275-591; E-mail: [email protected]
The research was supported by the Medical Research Council and the European Union Biotechnology Programme.
Received:
August 26 1998
Revision Received:
September 23 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1998
J Exp Med (1998) 188 (11): 2083–2090.
Article history
Received:
August 26 1998
Revision Received:
September 23 1998
Citation
Marion H. Brown, Kent Boles, P. Anton van der Merwe, Vinay Kumar, Porunelloor A. Mathew, A. Neil Barclay; 2B4, the Natural Killer and T Cell Immunoglobulin Superfamily Surface Protein, Is a Ligand for CD48 . J Exp Med 7 December 1998; 188 (11): 2083–2090. doi: https://doi.org/10.1084/jem.188.11.2083
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