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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2648-2654. Prepublished online as a Blood First Edition Paper on October 23, 2003; DOI 10.1182/blood-2003-07-2532. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-07-2532v1 103/7/2648    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 Moris, A. Articles by Schwartz, O. Search for Related Content PubMed PubMed Citation Articles by Moris, A. Articles by Schwartz, O. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY DC-SIGN promotes exogenous MHC-I–restricted HIV-1 antigen presentation Arnaud Moris, Cinzia Nobile, Florence Buseyne, Françoise Porrot, Jean-Pierre Abastado, and Olivier Schwartz From the Groupe Virus et Immunité and Unité d'Immunopathologie Virale, URA CNRS 1930, Institut Pasteur, Paris, France; and IDM Research Laboratories, Institut des Cordeliers, Paris, France. Dendritic cells (DCs) facilitate HIV-1 spread in the host by capturing virions and transferring them to permissive lymphocytes in lymphoid organs. Lectins such as DC-specific ICAM-grabbing non-integrin (DC-SIGN) are involved in HIV-1 uptake by DCs, through high-affinity binding to viral envelope glycoproteins. We examined the role of DC-SIGN on the fate of incoming virions and on major histocompatibility complex class I (MHC-I)–restricted HIV-1 antigen presentation. We show that DC-SIGN expression in B-cell lines dramatically enhances viral internalization. In these cells, and also in primary DCs, most of the captured virions are rapidly degraded, likely in a lysosomal compartment. In addition, a fraction of incoming viral material is processed by the proteasome, leading to activation of anti–HIV-specific cytotoxic T lymphocytes (CTLs) by DC-SIGN–expressing cells. In DCs, DC-SIGN is not the only receptor involved, and redundant pathways of virus capture leading to antigen presentation likely coexist. Altogether, our results highlight new aspects of DC-SIGN interactions with HIV-1. The lectin does not significantly protect captured virions against degradation and promotes MHC-I exogenous presentation of HIV-1 antigens. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Frank, H. Stossel, A. Gettie, S. G. Turville, J. W. Bess Jr., J. D. Lifson, I. Sivin, N. 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