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

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Item Type:Article
Title:Autophagy is a critical regulator of memory CD8(+) T cell formation
Creators Name:Puleston, D.J. and Zhang, H. and Powell, T.J. and Lipina, E. and Sims, S. and Panse, I. and Watson, A.S. and Cerundolo, V. and Townsend, A.R. and Klenerman, P. and Simon, A.K.
Abstract: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.
Keywords:Apoptosis, Autophagy, Autophagy-Related Protein 7, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Differentiation, Cell Proliferation, Cell Survival, Epitopes, Glucose Transporter Type 1, Immunologic Memory, Lymphocyte Count, Lymphocytic Choriomeningitis Virus, Microtubule-Associated Proteins, Mitochondria, Phenotype, Reactive Oxygen Species, Secondary Immunization, Viral Vaccines, Animals, Mice
Publisher:eLife Sciences Publications
Page Range:e03706
Date:11 November 2014
Additional Information:Copyright © 2014, Puleston et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Official Publication:https://doi.org/10.7554/eLife.03706
PubMed:View item in PubMed

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