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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.

Autophagy is a critical regulator of memory CD8 + T cell formation