Journal
CELL REPORTS
Volume 23, Issue 12, Pages 3512-3524Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.05.057
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Funding
- Rebecca L. Cooper Medical Research Foundation
- Sylvia and Charles Viertel Senior Medical Research Fellowship
- National Health and Medical Research Council (NHMRC) [AI1102792]
- NHMRC [AI1071916, AI1046333]
- University of Melbourne
- Monash University
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Age-associated decreases in primary CD8(+) T cell responses occur, in part, due to direct effects on naive CD8(+) T cells to reduce intrinsic functionality, but the precise nature of this defect remains undefined. Aging also causes accumulation of antigen-naive but semi-differentiated virtual memory (T-vM ) cells, but their contribution to age-related functional decline is unclear. Here, we show that T-vm cells are poorly proliferative in aged mice and humans, despite being highly proliferative in young individuals, while conventional naive T cells (T-N cells) retain proliferative capacity in both aged mice and humans. Adoptive transfer experiments in mice illustrated that naive CD8 T cells can acquire a proliferative defect imposed by the aged environment but age-related proliferative dysfunction could not be rescued by a young environment. Molecular analyses demonstrate that aged T-vm cells exhibit a profile consistent with senescence, marking an observation of senescence in an antigenically naive T cell population.
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