Extracellular Delivery of Functional Mitochondria Reverses the Dysfunction of CD4+ T Cells in Aging
CD4+ T cell function
The authors investigated whether aging-associated mitochondrial dysfunction could be abrogated by transferring young mitochondria into CD4+ T from old mice and whether such a transfer may improve CD4+ T function. They showed that CD4+ T cells from old mice had significantly higher MitoSOX compared to CD4+ T cells from young mice both at the basal state and after activation. Then they transferred mitochondria sourced from MEFs to CD4+ T from old mice and found that mitochondrial transfer improved the redox status, increased the rates of OXPHOS, glycolysis and function of CD4+ T cells from old mice ex vivo.
The authors did not answer a few fundamental questions:
Are all mitochondria transferred functional?
The fate of the transferred and the original mitochondria in the cells: fusion, degradation, rejection?
What CD4 population?
These findings support the idea that mitochondria can serve as targets for therapeutic intervention in ageing by opening the possibility of future translational studies on the immunological and therapeutic implications of directed mito-transfer in aged lymphocytes to restore their loss of function.
Reviewed by Ghada Alsaleh as part of the cross-institutional journal club of the Immunology Institute of the Icahn School of Medicine, Mount Sinai and the Kennedy Institute of Rheumatology, University of Oxford.