Elevated LDL-C induces T-cell metabolic dysfunction and increases inflammation and oxidative stress in mid-life adults.

Theodore M DeConne, Arit Ghosh, Catherine Awad, Ibra S Fancher, David G Edwards, Daniel W Trott, Christopher R Martens

Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE, USA.Department of Kinesiology and Applied Physiology, University of Delaware, Newark, DE, USA. · pubmed

Paper

Abstract

T-cells may contribute to chronic, low-grade, sustained inflammation and oxidative stress commonly observed with aging and chronic disease. T-cell metabolic alterations impact T-cell differentiation, inflammation, and oxidative stress in animal models. Low-density lipoprotein cholesterol (LDL-C) has been identified as a novel antigen that activates T-cells via a canonical pathway. However, in humans, little is known about the direct effect of LDL-C on T-cells. Endogenous LDL-C concentration peaks during mid-life in humans and may contribute to midlife chronic disease risk by inducing T-cell dysfunction. Thus, this study investigated the effects of exogenous LDL-C exposure on CD4

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Research summary

Elevated LDL-C exposure induces metabolic dysfunction in T-cells, contributing to inflammation and oxidative stress in mid-life adults. The study addresses the role of LDL-C in T-cell dysfunction, which may be a contributing factor to chronic diseases associated with aging, thus linking it to the root causes of age-related health issues.

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