Die mit dem ERC Consolidator Grant ausgezeichnete Forscherin gab Einblicke in die noch nicht veröffentlichten Ergebnisse ihres Grants "Let T Be":
As in many other cells and tissues, cells of the immune system present mitochondrial decline with age. 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 defective T cells contribute to inflammaging and age-related diseases and will discuss novel therapeutic opportunities to promote healthy aging.
