Myeloid marker expression on antiviral CD8+ T cells following an acute virus infection

Authors

  • Yinling Lin,

    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, USA
    2. The Walther Oncology Center, Indianapolis, USA
    3. The Walther Cancer Institute, Indianapolis, USA
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  • Tonya J. Roberts,

    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, USA
    2. The Walther Oncology Center, Indianapolis, USA
    3. The Walther Cancer Institute, Indianapolis, USA
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  • Venkataraman Sriram,

    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, USA
    2. The Walther Oncology Center, Indianapolis, USA
    3. The Walther Cancer Institute, Indianapolis, USA
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  • Sungyoo Cho,

    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, USA
    2. The Walther Oncology Center, Indianapolis, USA
    3. The Walther Cancer Institute, Indianapolis, USA
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  • Randy R. Brutkiewicz

    Corresponding author
    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, USA
    2. The Walther Oncology Center, Indianapolis, USA
    3. The Walther Cancer Institute, Indianapolis, USA
    • Department of Microbiology and Immunology, Indiana University School of Medicine, Building R2, Room 302, 950 W. Walnut St., Indianapolis, IN 46202–5181, USA Fax: +1-317-274-7592
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Abstract

CD11b, CD11c, and F4/80 are normally used to define dendritic cell and/or macrophage populations. In this study, the expression of all three markers was observed on CD8+ T cells following infection of mice with several distinct viruses. Using lymphocytic choriomeningitis virus as a model virus, it was found that relatively more CD11b+CD8+ and CD11c+CD8+ T cells were present in the periphery than in primary lymphoid organs; in contrast, the F4/80+CD8+ T cell population was more prevalent in the spleen. All three myeloid markers were detected on virus-specific CTL. The expression of CD11b and CD11c on CD8+ T cells correlated with their level of CTL activity, whereas the F4/80+CD8+ T cell population increased after the peak of the CTL response but did not have higher CTL activity. These data suggest that there is a differential induction of CD11b, CD11c, and F4/80 on virus-specific CD8+ T cells following an acute virus infection.

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