Description
We show that fat-resident regulatory T cells, termed fTregs, drive age-associated insulin resistance and can be specifically depleted to increase adipose insulin sensitivity. Comparative AdipoImmune profiling in young, aged, and obese mice reveals that fTregs progressively enrich in adipose as a function of age, but not obesity. fTreg-deficient mice are protected from age-associated insulin resistance and its accompanying physiological hallmarks. In contrast, fTreg-deficiency offers no protection from obesity-associated insulin resistance.