Decoding the contribution of the immune system to aging

Speaker: Maria Mittelbrunn Herrero
Institution: Inmunometabolism & Inflammation Lab, Centro de Biología Molecular Severo Ochoa, Madrid, Spain

Place: Jerónimo Forteza conference room, CIPF

Abstract: To investigate the consequences of the aging of the immune system, we have induced age-associated mitochondrial dysfunction prematurely in T cell. Targeting mitochondrial function in T cells recapitulates metabolic, phenotypic and functional features of aged T cells, including susceptibility to infections and premature inflammaging. We found that inducing age-associated mitochondrial decline in T lymphocytes, does not only cause an immunometabolic dysfunction that drives T cell senescence, but actually causes a general, body-wide deterioration of health with multiple aging-related features, including metabolic, musculoskeletal, cardiovascular and cognitive alterations, altogether resulting in premature death. Thus, premature aging of T lymphocytes may be ‘contagious’, driving a generalized acceleration of aging throughout multiple organ systems. Our results place the metabolism of T cells at the crossroad between inflammation, senescence and aging, highlighting that immunometabolism can be a therapeutic target to delay aging. This presentation will decode the molecular mechanism by which mitochondrial defective T cells contribute to inflammaging and age-related diseases and will discuss novel therapeutic opportunities to promote healthy aging.

Funding: This study was supported by the European Regional Development Fund (ERDF) and the European Commission through H2020-EU.1.1, European Research Council grant ERC-2021-CoG 101044248-LetTBe

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