Abstract
Mitochondrial dysfunction alters cellular metabolism, increases oxidative stress, and may be principal to the dysregulated signaling and function of CD4+ T lymphocytes in the elderly. Mitochondria influence adaptive immune responses through glucose and fatty acid metabolism, calcium buffering, and redox signaling. By transferring young mitochondria into CD4+ T cells from old mice, we investigated whether aging-associated mitochondrial dysfunction could be abrogated and whether such transfer changed CD4+ T cell function. Our results show that mitochondrial transfer improved the redox status and function of CD4+ T cells from old mice ex vivo. These findings support the notion that mitochondria can serve as targets of therapeutic intervention in aging.
Competing Interest Statement
The authors have declared no competing interest.
