New roles for autophagy and spermidine in T cells
Authors:D. J. Puleston and A. K. Simon
doi: 10.15698/mic2015.03.195
Volume 2, pp. 91 to 93, published 02/03/2015.
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS.
Keywords:
autophagy, T cell memory, spermidine, T cells, ageing, immunosenescence, immunity
Corresponding Author(s):
Conflict of interest statement:
The authors are named inventors on a UK patent application (No. 1404438.2) pertaining to the use of polyamines in the immune system.
Please cite this article as:
D. J. Puleston and A. K. Simon (2015). New roles for autophagy and spermidine in T cells. Microbial Cell 2(3): 91-93.
© 2015 Puleston and Simon. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
The conserved lysosomal degradation pathway autophagy is now recognised as an essential cog in immune function. While functionally widespread in the innate immune system, knowledge of its roles in adaptive immunity is more limited. Although autophagy has been implicated in naïve T cell homeostasis, its requirement in antigen-specific T cells during infection was unknown. Using a murine model where the essential autophagy gene Atg7 is deleted in the T cell lineage, we have shown that autophagy is dispensable for effector CD8+ T cell responses, but crucial for the formation of memory CD8+ T cells. Here, we suggest reasons why autophagy might be important for the formation of long-lasting immunity. Like in the absence of autophagy, T cell memory formation during ageing is also defective. We observed diminished autophagy levels in T cells from aged mice, linking autophagy to immunosenescence. Importantly, T cell responses to influenza vaccination could be significantly improved using the autophagy-inducing compound spermidine. These results suggest the autophagy pathway as a desirable target to improve aged immunity and modulate T cell function.