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Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-07-2103. This Article Full Text (PDF) All Versions of this Article: 2002-07-2103v1 101/7/2711    most recent Alert me when this article is cited Alert me if a correction is posted 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 Brenchley, J. M Articles by Koup, R. A Search for Related Content PubMed PubMed Citation Articles by Brenchley, J. M Articles by Koup, R. A Social Bookmarking                   What's this? Submitted July 15, 2002 Accepted November 8, 2002 Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells Jason M Brenchley, Nitin J Karandikar, Michael R Betts, David R Ambrozak, Brenna J Hill, Laura E Crotty, Joseph P Casazza, Janaki Kuruppu, Stephen A Migueles, Mark Connors, Mario Roederer, Daniel C Douek, and Richard A Koup* Department of Immunology, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes for Health, Bethesda, MD, USA Department of Pathology, UT Southwestern Medical Center, Dallas, TX, USA Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes for Health, Bethesda, MD, USA Experimental Transplantation and Immunology Branch, National Institute of Allergy and Infectious Diseases, National Institutes for Health, Bethesda, MD, USA * Corresponding author; email: rkoup{at}mail.nih.gov. Virus-specific CD8+ T-cell responses play a pivotal role in limiting viral replication. Alterations in these responses, such as decreased cytolytic function, inappropriate maturation, and limited proliferative ability could reduce their ability to control viral replication. Here, we report on the capacity of HIV-specific CD8+ T-cells to secrete cytokines and proliferate in response to HIV antigen stimulation. We find that a large proportion of HIV-specific CD8+ T-cells that produce cytokine in response to cognate antigen are unable to divide, and die during a 48 hour in vitro culture. This lack of proliferative ability of HIV-specific CD8+ T-cells is defined by surface expression of CD57, but not by absence of CD28 or CCR7. This inability to proliferate in response to antigen cannot be overcome by exogenous IL-2 or IL-15. Furthermore, CD57 expression on CD8+ T-cells, CD4+ T-cells and NK cells is a general marker of proliferative inability, a history of more cell divisions, and short telomeres. We suggest, therefore, that the increase in CD57+ HIV-specific CD8+ T-cells results from chronic antigen stimulation that is a hallmark of HIV infection. Thus, our studies define a phenotype associated with replicative senescence in HIV-specific CD8+ T-cells, which may have broad implications to other conditions associated with chronic antigenic stimulation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J.-S. Wang and C.-K. Wu Systemic hypoxia affects exercise-mediated antitumor cytotoxicity of natural killer cells J Appl Physiol, December 1, 2009; 107(6): 1817 - 1824. [Abstract] [Full Text] [PDF] T. K. Kim, L. S. St. John, E. D. Wieder, J. Khalili, Q. Ma, and K. V. 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