Journal
NATURE METABOLISM
Volume 2, Issue 10, Pages 1001-1012Publisher
NATURE RESEARCH
DOI: 10.1038/s42255-020-00280-9
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Funding
- European Research Council [802773-MitoGuide]
- Swiss National Science Foundation [31003A_182470]
- Swiss Institute for Experimental Cancer Research (ISREC) [26075483]
- Swiss Cancer League [KFS-3949-08-2016]
- Swiss Bridge Award
- Cancer Research Institute-CLIP Investigator award
- EMBO Young Investigator award
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Current immunotherapies yield remarkable clinical outcomes by boosting the power of host immunity in cancer cell elimination and viral clearance. However, after prolonged antigen exposure, CD8(+) T cells differentiate into a special differentiation state known as T-cell exhaustion, which poses one of the major hurdles to antiviral and antitumor immunity during chronic viral infection and tumour development. Growing evidence indicates that exhausted T cells undergo metabolic insufficiency with altered signalling cascades and epigenetic landscapes, which dampen effector immunity and cause poor responsiveness to immune-checkpoint-blockade therapies. How metabolic stress affects T-cell exhaustion remains unclear; therefore, in this Review, we summarize current knowledge of how T-cell exhaustion occurs, and discuss how metabolic insufficiency and prolonged stress responses may affect signalling cascades and epigenetic reprogramming, thus locking T cells into an exhausted state via specialized differentiation programming.
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