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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3524-3531. Prepublished online as a Blood First Edition Paper on July 26, 2005; DOI 10.1182/blood-2005-03-1243. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-03-1243v1 106/10/3524    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 Herbeuval, J.-P. Articles by Shearer, G. M. Search for Related Content PubMed PubMed Citation Articles by Herbeuval, J.-P. Articles by Shearer, G. M. Related Collections Immunobiology Apoptosis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY CD4+ T-cell death induced by infectious and noninfectious HIV-1: role of type 1 interferon–dependent, TRAIL/DR5-mediated apoptosis Jean-Philippe Herbeuval, Jean-Charles Grivel, Adriano Boasso, Andrew W. Hardy, Claire Chougnet, Matthew J. Dolan, Hideo Yagita, Jeffrey D. Lifson, and Gene M. Shearer From the Experimental Immunology Branch, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD; Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development (NICHD), NIH, Bethesda, MD; Division of Molecular Immunology, Children's Hospital Research Foundation, Cincinnati, OH; Infectious Diseases Service, Wilford Hall Medical Center, Lackland AFB, TX; Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan; and AIDS Vaccine Program, SAIC Frederick, Inc., NCI-Frederick, Frederick, MD. It has been proposed that direct and indirect mechanisms contribute to the unresolved issue of CD4+ T-cell depletion that results from HIV-1 infection. We recently reported that plasma levels of tumor necrosis factor (TNF)–related apoptosis-inducing ligand (TRAIL) are elevated in HIV-1–infected patients and that they correlate with viral load. The present study investigates the expression of TRAIL death receptor 5 (DR5) in the peripheral-blood mononuclear cells (PBMCs) of HIV-1–infected patients and its role in CD4+ T-cell death. DR5 expression was elevated and associated with the apoptotic marker annexin V. Apoptosis was reduced in CD4+ T cells when cultured with anti-DR5 antibody. CD4+, but not CD8+, T cells from uninfected donors expressed TRAIL, DR5, and activated caspase-3 when cultured with infectious or noninfectious HIV-1, resulting in preferential apoptosis of CD4+ T cells. TRAIL, caspase-3 expression, and apoptosis were type 1 interferon (IFN) dependent. Induction of apoptosis and DR5 expression required glycoprotein 120 (gp120)–CD4 interaction. Finally, we analyzed DR5 expression by CD4+ T cells in highly active antiretroviral therapy (HAART)–treated patients. The decreased viral loads and increased CD4 counts of HAART-responsive patients were associated with a decrease in DR5 mRNA expression by CD4+ T lymphocytes. We propose a novel model in which a type 1 IFN–regulated TRAIL /DR5 mechanism induces apoptosis of HIV-1–exposed CD4+ T cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Stary, I. Klein, S. Kohlhofer, F. Koszik, T. Scherzer, L. Mullauer, H. Quendler, N. Kohrgruber, and G. Stingl Plasmacytoid dendritic cells express TRAIL and induce CD4+ T-cell apoptosis in HIV-1 viremic patients Blood, October 29, 2009; 114(18): 3854 - 3863. [Abstract] [Full Text] [PDF] M. Meythaler, A. Martinot, Z. Wang, S. Pryputniewicz, M. Kasheta, B. Ling, P. A. Marx, S. O'Neil, and A. Kaur Differential CD4+ T-Lymphocyte Apoptosis and Bystander T-Cell Activation in Rhesus Macaques and Sooty Mangabeys during Acute Simian Immunodeficiency Virus Infection J. 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