Abstract：
:The AMP-activated kinase (AMPK) is a major energy sensor metabolic enzyme that is activated early during T cell immune responses but its role in the generation of effector T cells is still controversial. Using both in vitro and in vivo models of T cell proliferation, we show herein that AMPK is dispensable for early TCR signaling and short-term proliferation but required for sustained long-term T cell proliferation and effector/memory T cell survival. In particular, AMPK promoted accumulation of effector/memory T cells in competitive homeostatic proliferation settings. Transplantation of AMPK-deficient hematopoïetic cells into allogeneic host recipients led to a reduced graft-versus-host disease, further bolstering a role for AMPK in the expansion and pathogenicity of effector T cells. Mechanistically, AMPK expression enhances the mitochondrial membrane potential of T cells, limits reactive oxygen species (ROS) production, and resolves ROS-mediated toxicity. Moreover, dampening ROS production alleviates the proliferative defect of AMPK-deficient T cells, therefore indicating a role for an AMPK-mediated ROS control of T cell fitness.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Lepez A,Pirnay T,Denanglaire S,Perez-Morga D,Vermeersch M,Leo O,Andris Fdoi
10.1038/s41598-020-78715-2subject
Has Abstractpub_date
2020-12-10 00:00:00pages
21673issue
1issn
2045-2322pii
10.1038/s41598-020-78715-2journal_volume
10pub_type
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