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Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition
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Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition
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Journal Article
Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition
2018
Overview
Defining the suppressive mechanisms used by regulatory T (Treg) cells is critical for the development of effective strategies for treating tumors and chronic infections. The molecular processes that occur in responder T cells that are suppressed by Treg cells are unclear. Here we show that human Treg cells initiate DNA damage in effector T cells caused by metabolic competition during cross-talk, resulting in senescence and functional changes that are molecularly distinct from anergy and exhaustion. ERK1/2 and p38 signaling cooperate with STAT1 and STAT3 to control Treg-induced effector T-cell senescence. Human Treg-induced T-cell senescence can be prevented via inhibition of the DNA damage response and/or STAT signaling in T-cell adoptive transfer mouse models. These studies identify molecular mechanisms of human Treg cell suppression and indicate that targeting Treg-induced T-cell senescence is a checkpoint for immunotherapy against cancer and other diseases associated with Treg cells.
Regulatory T (Treg) cells can induce senescence of tumour-associated effector T cells, but it is not clear how. Here the authors show that Treg cells outcompete effector T cells for glucose uptake, resulting in activation of the DNA damage response in effector T cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/21
/ 13/31
/ 14
/ 14/32
/ 49
/ 49/109
/ 49/22
/ 49/61
/ 49/90
/ 96
/ Anergy
/ Cancer
/ DNA
/ Humanities and Social Sciences
/ Humans
/ Science
/ STAT1 Transcription Factor - metabolism
/ STAT1 Transcription Factor - physiology
/ STAT3 Transcription Factor - metabolism
/ STAT3 Transcription Factor - physiology
/ T-Lymphocytes, Regulatory - metabolism
/ T-Lymphocytes, Regulatory - physiology
/ Tumors
