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    The LCMV gp33-specific memory T cell repertoire narrows with age

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    Author
    Bunztman, Adam
    Vincent, Benjamin
    Krovi, Harsha
    Steele, Shaun
    Frelinger, Jeffrey
    Affiliation
    Department of Immunobiology, University of Arizona, Tucson, AZ, 85724, USA
    Departments of Medicine, University of North Carolina, Chapel Hill, NC, 27599, USA
    Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, 27599, USA
    Issue Date
    2012
    Keywords
    CD8 T cell
    T cell repertoire
    T cell receptor
    Aging
    
    Metadata
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    Publisher
    BioMed Central
    Citation
    Bunztman et al. Immunity & Ageing 2012, 9:17 http://www.immunityageing.com/content/9/1/17
    Journal
    Immunity & Ageing
    Rights
    © 2012 Bunztman et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
    Collection Information
    This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
    Abstract
    BACKGROUND:The memory response to LCMV in mice persists for months to years with only a small decrease in the number of epitope specific CD8 T cells. This long persistence is associated with resistance to lethal LCMV disease. In contrast to studies focused on the number and surface phenotype of the memory cells, relatively little attention has been paid to the diversity of TCR usage in these cells. CD8+ T cell responses with only a few clones of identical specificity are believed to be relatively ineffective, presumably due to the relative ease of virus escape. Thus, a broad polyclonal response is associated with an effective anti-viral CD8+ T cell response.RESULTS:In this paper we show that the primary CD8+ T cell response to the LCMV gp33-41 epitope is extremely diverse. Over time while the response remains robust in terms of the number of gp33-tetramer+ T cells, the diversity of the response becomes less so. Strikingly, by 26months after infection the response is dominated by a small number TCRbeta sequences. In addition, it is of note the gp33 specific CD8+ T cells sorted by high and low tetramer binding populations 15 and 22months after infection. High and low tetramer binding cells had equivalent diversity and were dominated by a small number of clones regardless of the time tested. A similar restricted distribution was seen in NP396 specific CD8+ T cells 26months after infection. The identical TCRVbeta sequences were found in both the tetramerhi and tetramerlo binding populations. Finally, we saw no evidence of public clones in the gp33-specific response. No CDR3 sequences were found in more than one mouse.CONCLUSIONS:These data show that following LCMV infection the CD8+ gp33-specific CD8 T cell response becomes highly restricted with enormous narrowing of the diversity. This narrowing of the repertoire could contribute to the progressively ineffective immune response seen in aging.
    EISSN
    1742-4933
    DOI
    10.1186/1742-4933-9-17
    Version
    Final published version
    Additional Links
    http://www.immunityageing.com/content/9/1/17
    ae974a485f413a2113503eed53cd6c53
    10.1186/1742-4933-9-17
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