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T Cell-Expressed microRNA-155 Reduces Lifespan in a Mouse Model of Age-Related Chronic Inflammation.

  • Author(s): Ekiz, H Atakan
  • Ramstead, Andrew G
  • Lee, Soh-Hyun
  • Nelson, Morgan C
  • Bauer, Kaylyn M
  • Wallace, Jared A
  • Hu, Ruozhen
  • Round, June L
  • Rutter, Jared
  • Drummond, Micah J
  • Rao, Dinesh S
  • O'Connell, Ryan M
  • et al.

Published Web Location

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325601/
No data is associated with this publication.
Abstract

Aging-related chronic inflammation is a risk factor for many human disorders through incompletely understood mechanisms. Aged mice deficient in microRNA (miRNA/miR)-146a succumb to life-shortening chronic inflammation. In this study, we report that miR-155 in T cells contributes to shortened lifespan of miR-146a-/- mice. Using single-cell RNA sequencing and flow cytometry, we found that miR-155 promotes the activation of effector T cell populations, including T follicular helper cells, and increases germinal center B cells and autoantibodies in mice aged over 15 months. Mechanistically, aerobic glycolysis genes are elevated in T cells during aging, and upon deletion of miR-146a, in a T cell miR-155-dependent manner. Finally, skewing T cell metabolism toward aerobic glycolysis by deleting mitochondrial pyruvate carrier recapitulates age-dependent T cell phenotypes observed in miR-146a-/- mice, revealing the sufficiency of metabolic reprogramming to influence immune cell functions during aging. Altogether, these data indicate that T cell-specific miRNAs play pivotal roles in regulating lifespan through their influences on inflammaging.

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