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

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 lysosom...

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Asıl Yazarlar: Puleston, D, Zhang, H, Powell, T, Lipina, E, Sims, S, Panse, I, Watson, A, Cerundolo, V, Townsend, A, Klenerman, P, Simon, A
Materyal Türü: Journal article
Dil:English
Baskı/Yayın Bilgisi: eLife Sciences Publications 2014
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author Puleston, D
Zhang, H
Powell, T
Lipina, E
Sims, S
Panse, I
Watson, A
Cerundolo, V
Townsend, A
Klenerman, P
Simon, A
author_facet Puleston, D
Zhang, H
Powell, T
Lipina, E
Sims, S
Panse, I
Watson, A
Cerundolo, V
Townsend, A
Klenerman, P
Simon, A
author_sort Puleston, D
collection OXFORD
description 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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spelling oxford-uuid:9689d241-9dce-4145-9af9-2189afa1a5772022-03-26T23:53:38ZAutophagy is a critical regulator of memory CD8(+) T cell formation.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:9689d241-9dce-4145-9af9-2189afa1a577EnglishSymplectic Elements at OxfordeLife Sciences Publications2014Puleston, DZhang, HPowell, TLipina, ESims, SPanse, IWatson, ACerundolo, VTownsend, AKlenerman, PSimon, ADuring 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.
spellingShingle Puleston, D
Zhang, H
Powell, T
Lipina, E
Sims, S
Panse, I
Watson, A
Cerundolo, V
Townsend, A
Klenerman, P
Simon, A
Autophagy is a critical regulator of memory CD8(+) T cell formation.
title Autophagy is a critical regulator of memory CD8(+) T cell formation.
title_full Autophagy is a critical regulator of memory CD8(+) T cell formation.
title_fullStr Autophagy is a critical regulator of memory CD8(+) T cell formation.
title_full_unstemmed Autophagy is a critical regulator of memory CD8(+) T cell formation.
title_short Autophagy is a critical regulator of memory CD8(+) T cell formation.
title_sort autophagy is a critical regulator of memory cd8 t cell formation
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