Extracellular Delivery of Functional Mitochondria Reverses the Dysfunction of CD4+ T Cells in Aging

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.