This summer our newest report “T cells mediate cell non-autonomous arterial ageing in mice” was published in Journal of Physiology and selected as an ‘Editors Choice!’ We found that T cells accumulate with age around both the aorta and mesenteric arteries and that with age there is a shift towards proinflammatory CD8+ effector memory cells around the arteries. To determine a causal role of T cells in arterial dysfunction, we found that 28 days of treatment with antibody fragments to deplete T cells resulted in improvement in existing age-related aortic stiffness and resulted in greater endothelium dependent dilation in the mesenteric arteries. We also examined large artery stiffness throughout life and found that Rag-1-/- mice, which don’t have T cells exhibit blunted increases in aortic stiffness and preserved endothelium dependent dilation. This investigation provides evidence that T cells can mediate arterial dysfunction in the absence of supraphysiological stimuli (i.e. angiotensin II) or genetic models (i.e. deletion of ApoE or Ldlr) of atherosclerosis. Collectively, these results indicate that T cells are major contributors to both large elastic artery and resistance arteriolar dysfunction with age.
