Journal
SCIENCE
Volume 368, Issue 6497, Pages 1371-+Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax0860
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Funding
- Fondo de Investigacion Sanitaria del Instituto de Salud Carlos III [PI16/02188, PI19/00855, PI16/02110]
- European Regional Development Fund (ERDF)
- European Commission through H2020-EU.1.1
- European Research Council [ERC-2016-StG 715322-EndoMitTalk]
- Comunidad de Madrid [S2017/BMD-3867 RENIM-CM, 2017-T2/BMD-5766]
- FPI-UAM
- Juan de la Cierva [FJCI-2017-33855, IJC2018-036850]
- UAM [2017-T2/BMD-5766]
- ERC [ERC-2018-CoG 819775-MATRIX]
- Miguel Servet Program [CPII 19/00014]
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The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (inflammaging). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-a signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases.
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