Abstract
PURPOSE OF REVIEW: The majority of leukocytes in advanced human atherosclerotic plaques are T-cells. T-cell subsets exert pro- or anti-atherogenic effects largely via the cytokines they secrete. T regulatory cells (T regs) are anti-inflammatory, but may lose these properties during atherosclerosis, proposed to be downstream of cholesterol accumulation. Aged T-cells also accumulate cholesterol. The effects of T-cell cholesterol accumulation on T-cell fate and atherosclerosis are not uniform.
RECENT FINDINGS: T-cell cholesterol accumulation enhances differentiation into pro-atherogenic cytotoxic T-cells and boosts their killing capacity, depending on the localization and extent of cholesterol accumulation. Excessive cholesterol accumulation induces T-cell exhaustion or T-cell apoptosis, the latter decreasing atherosclerosis but impairing T-cell functionality in terms of killing capacity and proliferation. This may explain the compromised T-cell functionality in aged T-cells and T-cells from CVD patients. The extent of T-cell cholesterol accumulation and its cellular localization determine T-cell fate and downstream effects on atherosclerosis and T-cell functionality.
Original language | English |
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Pages (from-to) | 527-534 |
Number of pages | 8 |
Journal | Current atherosclerosis reports |
Volume | 25 |
Issue number | 9 |
DOIs | |
Publication status | Published - Sept-2023 |
Keywords
- Humans
- Aged
- Atherosclerosis
- Plaque, Atherosclerotic
- Cholesterol
- T-Lymphocytes
- Aging