Identification of DC-SIGN, a Novel Dendritic Cell–Specific ICAM-3 Receptor that Supports Primary Immune Responses

• Published in: Cell Vol. 100; no. 5; pp. 575 - 585
• Main Authors: Geijtenbeek, Teunis B.H, Torensma, Ruurd, van Vliet, Sandra J, van Duijnhoven, Gerard C.F, Adema, Gosse J, van Kooyk, Yvette, Figdor, Carl G
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 03.03.2000
• Subjects: AIDS/HIV; Animals; Antibodies, Monoclonal - pharmacology; Antigen Presentation; Antigens - metabolism; Antigens, CD; Antigens, Differentiation; Calcium - physiology; Cell Adhesion; Cell Adhesion Molecules - immunology; Cell Adhesion Molecules - isolation & purification; Cell Adhesion Molecules - metabolism; Cell Communication; Cells, Cultured; DC-SIGN protein; Dendritic Cells - immunology; Flow Cytometry; Gene Expression; Humans; intercellular adhesion molecule 3; Intercellular Adhesion Molecule-1 - physiology; K562 Cells; Lectins - immunology; Lectins - physiology; Lectins, C-Type; Lymphocyte Activation - physiology; Lymphocyte Function-Associated Antigen-1 - physiology; Mannans - pharmacology; Mannose - metabolism; Mice; Mice, Inbred BALB C; Models, Immunological; Molecular Weight; Receptors, Cell Surface - immunology; Receptors, Cell Surface - physiology; Receptors, HIV - isolation & purification; Recombinant Fusion Proteins - physiology; T-Lymphocytes - cytology; T-Lymphocytes - immunology; Transfection
• ISSN: 0092-8674; 1097-4172
• DOI: 10.1016/S0092-8674(00)80693-5

Contact between dendritic cells (DC) and resting T cells is essential to initiate a primary immune response. Here, we demonstrate that ICAM-3 expressed by resting T cells is important in this first contact with DC. We discovered that instead of the common ICAM-3 receptors LFA-1 and αDβ2, a novel DC-specific C-type lectin, DC-SIGN, binds ICAM-3 with high affinity. DC-SIGN, which is abundantly expressed by DC both in vitro and in vivo, mediates transient adhesion with T cells. Since antibodies against DC-SIGN inhibit DC-induced proliferation of resting T cells, our findings predict that DC-SIGN enables T cell receptor engagement by stabilization of the DC–T cell contact zone.