Journal
ELIFE
Volume 3, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.03706
Keywords
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Categories
Funding
- Medical Research Council Human Immunology Unit, Oxford
- Wellcome Trust [088098/Z/08/Z]
- Allan and Nesta Ferguson Charitable Trust
- Natural Sciences and Engineering Research Council of Canada
- Lady Tata Memorial Trust
- Wellcome Trust [088098/Z/08/Z] Funding Source: Wellcome Trust
- BBSRC [BB/G021422/1] Funding Source: UKRI
- MRC [MC_UU_12010/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G021422/1] Funding Source: researchfish
- Cancer Research UK [11331] Funding Source: researchfish
- Medical Research Council [MC_UU_12010/1] Funding Source: researchfish
- Wellcome Trust [103830/Z/14/Z] Funding Source: researchfish
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During infection, CD8(+) T cells initially expand then contract, leaving a small memory pool providing long lasting immunity. While it has been described that CD8(+) T cell memory formation becomes defective in old age, the cellular mechanism is largely unknown. Autophagy is a major cellular lysosomal degradation pathway of bulk material, and levels are known to fall with age. In this study, we describe a novel role for autophagy in CD8(+) T cell memory formation. Mice lacking the autophagy gene Atg7 in T cells failed to establish CD8(+) T cell memory to influenza and MCMV infection. Interestingly, autophagy levels were diminished in CD8(+) T cells from aged mice. We could rejuvenate CD8(+) T cell responses in elderly mice in an autophagy dependent manner using the compound spermidine. This study reveals a cell intrinsic explanation for poor CD8(+) T cell memory in the elderly and potentially offers novel immune modulators to improve aged immunity.
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