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      DC-SIGN (CD209) Mediates Dengue Virus Infection of Human Dendritic Cells

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          Abstract

          Dengue virus is a single-stranded, enveloped RNA virus that productively infects human dendritic cells (DCs) primarily at the immature stage of their differentiation. We now find that all four serotypes of dengue use DC-SIGN (CD209), a C-type lectin, to infect dendritic cells. THP-1 cells become susceptible to dengue infection after transfection of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), or its homologue L-SIGN, whereas the infection of dendritic cells is blocked by anti–DC-SIGN antibodies and not by antibodies to other molecules on these cells. Viruses produced by dendritic cells are infectious for DC-SIGN– and L-SIGN–bearing THP-1 cells and other permissive cell lines. Therefore, DC-SIGN may be considered as a new target for designing therapies that block dengue infection.

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          Identification of DC-SIGN, a novel dendritic cell-specific ICAM-3 receptor that supports primary immune responses.

          T B H Geijtenbeek, R Torensma, S. van Vliet … (2000)
          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 alphaDbeta2, 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.
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            Mycobacteria Target DC-SIGN to Suppress Dendritic Cell Function

            Teunis Geijtenbeek, Sandra J. van Vliet, Estella Koppel … (2003)
            Mycobacterium tuberculosis represents a world-wide health risk and immunosuppression is a particular problem in M. tuberculosis infections. Although macrophages are primarily infected, dendritic cells (DCs) are important in inducing cellular immune responses against M. tuberculosis. We hypothesized that DCs represent a target for M. tuberculosis and that the observed immuno-suppression results from modulation of DC functions. We demonstrate that the DC-specific C-type lectin DC-SIGN is an important receptor on DCs that captures and internalizes intact Mycobacterium bovis bacillus Calmette-Guérin (BCG) through the mycobacterial cell wall component ManLAM. Antibodies against DC-SIGN block M. bovis BCG infection of DCs. ManLAM is also secreted by M. tuberculosis–infected macrophages and has been implicated as a virulence factor. Strikingly, ManLAM binding to DC-SIGN prevents mycobacteria- or LPS-induced DC maturation. Both mycobacteria and LPS induce DC maturation through Toll-like receptor (TLR) signaling, suggesting that DC-SIGN, upon binding of ManLAM, interferes with TLR-mediated signals. Blocking antibodies against DC-SIGN reverse the ManLAM-mediated immunosuppressive effects. Our results suggest that M. tuberculosis targets DC-SIGN both to infect DCs and to down-regulate DC-mediated immune responses. Moreover, we demonstrate that DC-SIGN has a broader pathogen recognition profile than previously shown, suggesting that DC-SIGN may represent a molecular target for clinical intervention in infections other than HIV-1.
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              Antibody-enhanced dengue virus infection in primate leukocytes.

              S B Halstead, E. O'Rourke (1977)
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exp Med
                Title: The Journal of Experimental Medicine
                Publisher: The Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date (Print): 7 April 2003
                Volume: 197
                Issue: 7
                Pages: 823-829
                Affiliations
                [1 ]Division of Retrovirology, Walter Reed Army Institute of Research and Henry M. Jackson Foundation for the Advancement of Military Medicine Diseases, Rockville, MD 20850
                [2 ]Viral Diseases Department, Naval Medical Research Center, Silver Spring, MD 20889
                [3 ]Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021
                [4 ]Department of Virus Diseases, Walter Reed Army Institute of Research, Silver Spring, MD 20889
                [5 ]Division of Instruments for Research, Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
                [6 ]Department of Immunology, Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
                Author notes

                Address correspondence to Mary A. Marovich, 13 Taft Ct., Suite 200, Rockville, MD 20850. Phone: 301 251-8337; Fax: 301 762-4177; E-mail: mmarovich@ 123456hivresearch.org

                Article
                Publisher ID: 20021840
                DOI: 10.1084/jem.20021840
                PMC ID: 2193896
                PubMed ID: 12682107
                SO-VID: 1f7708a9-d584-447e-b2cf-805ffce1af58
                Copyright © Copyright © 2003, The Rockefeller University Press
                History
                Date received : 22 October 2002
                Date revision received : 29 December 2002
                Date accepted : 28 January 2003
                Categories
                Subject: Article

                ScienceOpen disciplines: Medicine
                Keywords: lectin,receptor,virus receptor,antigen-presenting cells,flavivirus
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: lectin, receptor, virus receptor, antigen-presenting cells, flavivirus

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