T cells with dysfunctional mitochondria induce multimorbidity and premature senescence

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–α 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.

Source: ScienceNOW - June 17, 2020 Category: Science Authors: Desdin-Mico, G., Soto-Heredero, G., Aranda, J. F., Oller, J., Carrasco, E., Gabande-Rodriguez, E., Blanco, E. M., Alfranca, A., Cusso, L., Desco, M., Ibanez, B., Gortazar, A. R., Fernandez-Marcos, P., Navarro, M. N., Hernaez, B., Alcami, A., Baixauli, F., Tags: Immunology, Medicine, Diseases reports Source Type: news