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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1299-1307. Prepublished online as a Blood First Edition Paper on June 9, 2008; DOI 10.1182/blood-2008-01-136473. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-01-136473v1 112/4/1299    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lambert, A. A. Articles by Tremblay, M. J. Search for Related Content PubMed PubMed Citation Articles by Lambert, A. A. Articles by Tremblay, M. J. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY The C-type lectin surface receptor DCIR acts as a new attachment factor for HIV-1 in dendritic cells and contributes to trans- and cis-infection pathways Alexandra A. Lambert1, Caroline Gilbert2, Manon Richard3, André D. Beaulieu3, and Michel J. Tremblay1 1 Centre de Recherche en Infectiologie, 2 Centre de Recherche en Rhumatologie et Immunologie, and 3 Laboratoire de recherche sur l'Arthrite et l'Inflammation, Centre Hospitalier de l'Université Laval, and Faculté de Médecine, Université Laval, Québec, QC The dynamic interplay between dendritic cells (DCs) and human immunodeficiency virus type-1 (HIV-1) is thought to result in viral dissemination and evasion of antiviral immunity. Although initial observations suggested that the C-type lectin receptor (CLR) DC-SIGN was responsible for the trans-infection function of the virus, subsequent studies demonstrated that trans-infection of CD4+ T cells with HIV-1 can also occur through DC-SIGN–independent mechanisms. We demonstrate that a cell surface molecule designated DCIR (for DC immunoreceptor), a member of a recently described family of DC-expressing CLRs, can participate in the capture of HIV-1 and promote infection in trans and in cis of autologous CD4+ T cells from human immature monocyte-derived DCs. The contribution of DCIR to these processes was revealed using DCIR-specific siRNAs and a polyclonal antibody specific for the carbohydrate recognition domain of DCIR. Data from transfection experiments indicated that DCIR acts as a ligand for HIV-1 and is involved in events leading to productive virus infection. Finally, we show that the neck domain of DCIR is important for the DCIR-mediated effect on virus binding and infection. These results point to a possible role for DCIR in HIV-1 pathogenesis by supporting the productive infection of DCs and promoting virus propagation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. C. Hatch, J. Archer, and S. Gummuluru Glycosphingolipid Composition of Human Immunodeficiency Virus Type 1 (HIV-1) Particles Is a Crucial Determinant for Dendritic Cell-Mediated HIV-1 trans-Infection J. Virol., April 15, 2009; 83(8): 3496 - 3506. [Abstract] [Full Text] [PDF]

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