CD31 is a 130-kD glycoprotein of the immunoglobulin (Ig) superfamily expressed on the surface of endothelial cells, platelets, and several leukocyte subsets. Previous reports indicated that CD31 can mediate intercellular adhesion via both homophilic and heterophilic interaction mechanisms. Using a soluble recombinant CD31-Ig fusion protein (CD31 receptor globulin [Rg]), we demonstrate here that human CD31- T lymphocytes and CD4+CD31- T cell clones express a heterophilic CD31 ligand that is upregulated 18 h after activation. Interaction of CD31Rg with CD31- T helper cell (Th) clones was divalent cation independent but could be blocked by heparin, thus indicating that the CD31 counterreceptor on T cells can be distinguished from the ligands identified on other cell types. Moreover, a single chain protein of 120 kD was precipitated by CD31Rg from the lysates of CD31- Th clones. CD31Rg completely downregulated the proliferative response and cytokine production (interleukin-4, interferon-gamma, and tumor necrosis factor-alpha) of CD31- Th clones when the cells were maximally stimulated via immobilized CD3 monoclonal antibody. These results suggest that interaction of CD31 with a heterophilic counterreceptor on T lymphocytes can interfere with a positive regulatory pathway of T cell activation, or directly signal T cells to downregulate immune function.
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1 July 1996
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July 01 1996
Interaction of CD31 with a heterophilic counterreceptor involved in downregulation of human T cell responses.
E Prager,
E Prager
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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R Sunder-Plassmann,
R Sunder-Plassmann
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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C Hansmann,
C Hansmann
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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C Koch,
C Koch
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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W Holter,
W Holter
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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W Knapp,
W Knapp
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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H Stockinger
H Stockinger
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
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E Prager
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
R Sunder-Plassmann
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
C Hansmann
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
C Koch
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
W Holter
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
W Knapp
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
H Stockinger
Institute of Immunology, Vienna International Research Cooperation Center at Sandoz Forschunginstitut, University of Vienna, Austria.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1996) 184 (1): 41–50.
Citation
E Prager, R Sunder-Plassmann, C Hansmann, C Koch, W Holter, W Knapp, H Stockinger; Interaction of CD31 with a heterophilic counterreceptor involved in downregulation of human T cell responses.. J Exp Med 1 July 1996; 184 (1): 41–50. doi: https://doi.org/10.1084/jem.184.1.41
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