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Regulatory T cells suppress the expression of COX-2 in vulnerable plaque

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Abstract

COX-2 contributes to local inflammation in atherosclerotic lesions. Regulatory T cells (Tregs) enhance the stability of atherosclerotic plaques. The aim of this study was to detect the potential relationship between Tregs and COX-2 in vulnerable plaques. Thirty ApoE −/− mice were fed a high-fat diet, and a silastic perivascular collar was placed around the right common carotid artery to induce vulnerable plaques. Eight weeks after collar placement, the mice were divided randomly into three groups: control, PBS, and Treg groups. Four weeks later, the right common carotid arteries were collected to detect the expression of COX-2. The results showed that Tregs significantly suppressed the expression of COX-2 in vulnerable plaques. In an in vitro experiment, RAW264.7 cells were divided randomly into three groups, which were precultured without T cells or with CD4 + CD25- T cells or Tregs for 48 h with an anti-CD3 antibody; then the cells were stimulated with LPS for 24 h. The RAW264.7 cells were harvested for RT-PCR and western blot assays and the results showed that Tregs downregulated COX-2 expression in RAW264.7 cells. Therefore, Tregs inhibited the expression of COX-2 in vulnerable plaques and macrophages, and COX-2 inhibition may be an important effect of Tregs that results in atherosclerotic plaque stabilization.

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Acknowledgements

Sources of funding: this work was supported by the National 973 Basic Research Program of China (No. 2013CB530703 and No. 2015CB553604), the Program of Introducing Talents of Discipline to Universities (No. B07035), the State Key Program of National Natural Science of China (No. 61331001 and No.81530014), the International Collaboration and Exchange Program of China (No. 81320108004) and the Grants of the National Natural Science Foundation of China (No. 81425004, No. 81500340 and No. 81400195).

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Correspondence to Xiao Meng.

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Zhang, K., Kong, J., Liu, B. et al. Regulatory T cells suppress the expression of COX-2 in vulnerable plaque. Heart Vessels 35, 278–283 (2020). https://doi.org/10.1007/s00380-019-01491-1

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