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J Immunol. 2010 May 1;184(9):5151-9. doi: 10.4049/jimmunol.0902063. Epub 2010 Apr 5.

Cell-intrinsic defects in the proliferative response of antiviral memory CD8 T cells in aged mice upon secondary infection.

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  • 1Immunology Program, The Wistar Institute, Philadelphia, PA 19104, USA.

Abstract

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.

PMID:
20368274
DOI:
10.4049/jimmunol.0902063
[PubMed - indexed for MEDLINE]
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