Datasets

Title	Ribosome profiling of GC7/vehicle-treated mouse primary B cells
Organism
Number of Samples	8
Release Date	2019/07/08 00:00
Sequencing Types
Protocol Details

Title
Authors	Zhang H, Alsaleh G, Feltham J, Sun Y, Napolitano G, Riffelmacher T, Charles P, Frau L, Hublitz P, Yu Z, Mohammed S, Ballabio A, Balabanov S, Mellor J, Simon AK
Journal	Molecular cell
Publication Date	2019 Oct 3
Abstract	Failure to make adaptive immune responses is a hallmark of aging. Reduced B cell function leads to poor vaccination efficacy and a high prevalence of infections in the elderly. Here we show that reduced autophagy is a central molecular mechanism underlying immune senescence. Autophagy levels are specifically reduced in mature lymphocytes, leading to compromised memory B cell responses in old individuals. Spermidine, an endogenous polyamine metabolite, induces autophagy in vivo and rejuvenates memory B cell responses. Mechanistically, spermidine post-translationally modifies the translation factor eIF5A, which is essential for the synthesis of the autophagy transcription factor TFEB. Spermidine is depleted in the elderly, leading to reduced TFEB expression and autophagy. Spermidine supplementation restored this pathway and improved the responses of old human B cells. Taken together, our results reveal an unexpected autophagy regulatory mechanism mediated by eIF5A at the translational level, which can be harnessed to reverse immune senescence in humans. Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
PMC	PMC6863385
PMID	31474573
DOI

Zhang et al. 2019 (PRJNA553160)