Spermidine disrupts mitochondrial respiration and redox homeostasis in aged CD44+ CD49d− CD8+ T cells

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ID: 338067
2026
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Abstract
Spermidine (SPD) is a polyamine metabolite with anti-aging and immunomodulatory properties. We previously reported that SPD enhances mitochondrial respiration in CD44- CD8+ naïve T cells through the upregulation of fatty acid oxidation (FAO). However, the effects of SPD on CD44+ CD8+ effector T cells remain unknown. We found that SPD suppressed mitochondrial oxygen consumption rate (OCR) in CD44+ CD8+ T cells from aged mice, in contrast to its effects on those from young mice. This FAO-dependent reduction in respiration was associated with mitochondrial oxidative stress and accompanied by reduced IFN-γ production and proliferative capacity. Notably, within the aged CD44+ CD8+ T cell compartment, senescence-like CD44+ CD49d- subset (CD49d- cells)-predominantly accumulated with age-exhibited a marked decrease in OCR following SPD treatment, whereas CD44+ CD49d+ CD8+ T cells (CD49d+ cells) were unaffected. In CD49d- cells, SPD treatment disrupted redox balance as evidenced by reduced intracellular reduced-thiol levels with unchanged mitochondrial reactive oxygen species (ROS) levels, suggesting consumption of antioxidant reserves. SPD also induced structural remodeling of mitochondria in CD49d- cells, characterized by a shift toward shorter, more fragmented mitochondria with wider cristae spacing than in CD49d+ cells. In summary, our findings reveal that SPD paradoxically compromises mitochondrial respiration in a specific subset of aged CD8+ T cells by perturbing fatty acid metabolism and redox homeostasis.
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Authors Jun Wang, Yu Wang, Koki Ichimaru, Aprilia Maharani, Yasuharu Haku, Jiaxin Gu, Mai Kiyono, Keiko Yurimoto, Tomonori Yaguchi, Tasuku Honjo, Koji Kitaoka, Kenji Chamoto
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Journal international immunology
Year 2026
DOI
10.1093/intimm/dxag057
URL
https://doi.org/10.1093/intimm/dxag057
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