Cell reports · 2026
Inflammaging in aged tissues drives remodeling of the CD8+ T cell compartment.
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Shchukina Irina, Rodriguez-Hernandez Carlos J, Ruiz Heather S, Kleverov Maksim, Mintz Rachel L, Mineura Katsutaka, Gunawardana Subhadra C, Hsiung Sunnie, Bhattarai Bishan, Vachova Veronika, Kossl Jan, Mogilenko Denis A, Field Rachael L, Nguyen Tran H, Alayo Quazim A, Huckstep Christopher G, Vander Wielen Barbora, Brestoff Jonathan R, Stewart Sheila A, Piston David W, Egawa Takeshi, Kreisel Daniel, Randolph Gwendalyn J, Artyomov Maxim N
Аннотация
Aging strongly impacts CD8+ T cells, including the loss of naive cells and the emergence of age-associated GZMK+CD8+ T cells (TAA cells). Although TAA cells constitute a major population in aged mice, the pathway underlying their differentiation remains unknown. Here, we demonstrate that TAA cell development is cell extrinsic and requires antigen exposure within aged non-lymphoid tissues. Using a TNFΔ69AU/+ mouse model, we show that low-grade inflammation accelerates CD8+ T cell aging and promotes early accumulation of TAA cells. Analysis of TAA cell heterogeneity further identifies a progenitor subpopulation enriched in the aged adipose tissue. Finally, heterochronic transplantation experiments suggest that the aged adipose tissue can serve as a systemic source of TAA cells and contribute to the conversion of young CD8+ T cells into the aged phenotype. Together, these findings indicate that aged non-lymphoid tissues actively drive CD8+ T cell remodeling and identify adipose tissue as an important niche shaping immune aging.