Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells

DOI PDF 被引用文献14件
  • Jason M. Brenchley
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Nitin J. Karandikar
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Michael R. Betts
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • David R. Ambrozak
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Brenna J. Hill
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Laura E. Crotty
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Joseph P. Casazza
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Janaki Kuruppu
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Stephen A. Migueles
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Mark Connors
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Mario Roederer
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Daniel C. Douek
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.
  • Richard A. Koup
    From the Vaccine Research Center and the Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and the Experimental Transplantation and Immunology Branch, NCI, NIH, Bethesda, MD; and the Departments of Pathology and Neurology, University of Texas, Southwestern Medical Center, Dallas.

抄録

<jats:p>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 cytokines 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 interleukin-2 (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.</jats:p>

収録刊行物

  • Blood

    Blood 101 (7), 2711-2720, 2003-04-01

    American Society of Hematology

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