Therapeutic Immune Reprogramming by Rapamycin Attenuates Plaque Inflammation and Lymphoid Immune Responses in Aged Atherosclerotic Mice.

Jill de Mol, Daphne H de Korte, Marie A C Depuydt, Virginia Smit, Mireia N A Bernabé Kleijn, Peter J van Santbrink, Christoph J Binder, Florentina Porsch, Frank H Schaftenaar, Amanda C Foks

Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, the Netherlands.Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, the Netherlands. · pubmed

Paper

Abstract

Aging is a major risk factor for atherosclerosis and is accompanied by profound changes in the immune system, including effector T cell expansion, senescent cell accumulation, and increased pro-inflammatory signaling. Rapamycin, a promising rejuvenation therapeutic that inhibits mTORC1 and modulates immune aging, was investigated for its potential to attenuate pro-atherogenic immune responses in aged atherosclerotic mice. 80- to 90-week-old male Ldlr

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Research summary

Rapamycin treatment attenuates pro-atherogenic immune responses and plaque inflammation in aged atherosclerotic mice by reprogramming the immune system. This is relevant because it investigates a specific geroprotective intervention (mTOR inhibition) to mitigate age-related immune dysfunction (immunosenescence) and its downstream pathological consequences, rather than merely treating the symptom of atherosclerosis.

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