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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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MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.


CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Mitochondria, Animals, Mice, Lymphocytic choriomeningitis virus, Reactive Oxygen Species, Microtubule-Associated Proteins, Viral Vaccines, Epitopes, Lymphocyte Count, Immunization, Secondary, Apoptosis, Cell Differentiation, Cell Proliferation, Cell Survival, Immunologic Memory, Phenotype, Autophagy, Glucose Transporter Type 1, Autophagy-Related Protein 7