Cell-Intrinsic Defects in the Proliferative Response of Antiviral Memory CD8 T Cells in Aged Mice upon Secondary Infection
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- Vilma Decman
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Brian J. Laidlaw
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Lauren J. DiMenna
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Sarah Abdulla
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Krystyna Mozdzanowska
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Jan Erikson
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- Hildegund C. J. Ertl
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
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- E. John Wherry
- Immunology Program, The Wistar Institute, Philadelphia, PA 19104
説明
<jats:title>Abstract</jats:title> <jats:p>Although previous studies have demonstrated delayed viral clearance and blunted effector T cell responses in aged mice during infection, memory CD8 T cells and especially secondary responses have received less attention. In this study, we show that modest differences in the number of memory CD8 T cells formed in aged versus young animals were associated with altered memory CD8 T cell differentiation. Aged immune mice had increased morbidity and mortality upon secondary viral challenge, suggesting changes in T cell immunity. Indeed, virus-specific memory CD8 T cells from aged mice showed substantially reduced proliferative expansion upon secondary infection using multiple challenge models. In addition, this defect in recall capacity of aged memory CD8 T cells was cell-intrinsic and persisted upon adoptive transfer into young mice. Thus, the poor proliferative potential of memory T cells and altered memory CD8 T cell differentiation could underlie age-related defects in antiviral immunity.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 184 (9), 5151-5159, 2010-05-01
The American Association of Immunologists