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Increased Th17 Cell Frequency Concomitant with Decreased Foxp3+ Treg Cell Frequency in the Peripheral Circulation of Patients with Carotid Artery Plaques

Overview
Journal Inflamm Res
Date 2012 Jun 26
PMID 22728962
Citations 27
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Abstract

Objective And Design: We investigated a possible imbalance between T helper (Th)17 and CD4+ CD25+ forkhead/winged helix transcription factor (Foxp3) T regulatory (Treg) cells in patients with carotid artery plaques.

Material Or Subjects: From November 2009 to September 2010, we enrolled 126 males and 104 females with mean age 68.24 ± 6.71 years.

Treatment: Based on carotid artery sonography, the 230 subjects were categorized into three groups: plaque negative; stable plaques; and unstable plaques.

Methods: Th17 and Treg cell frequencies, relevant plasma cytokines (IL-17, IL-6, IL-23, and TNF-α), and RORγt mRNA levels were determined.

Results: Compared to plaque negative, Th17 cells, Th17-related cytokines (IL-17, IL-6, IL-23, and TNF-α), and RORγt mRNA levels were higher with stable plaques, and highest with unstable plaques. The opposite trend was found for Treg cells, Treg-related cytokines (IL-10 and TGF-β1), and Foxp3 mRNA. Th17 cell frequencies were significantly negatively correlated with Treg cell frequencies.

Conclusions: Our investigation demonstrated that there is a Th17/Treg functional imbalance in patients with unstable carotid atherosclerotic plaques. Th17 cells may promote atherogenesis, while Treg cells may have a protective role against atherosclerosis plaques. An imbalance of Th17/Treg cells may offer a new direction for the treatment of atherosclerosis.

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References
1.
Sauer S, Bruno L, Hertweck A, Finlay D, Leleu M, Spivakov M . T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR. Proc Natl Acad Sci U S A. 2008; 105(22):7797-802. PMC: 2409380. DOI: 10.1073/pnas.0800928105. View

2.
Daugherty A, Rateri D . T lymphocytes in atherosclerosis: the yin-yang of Th1 and Th2 influence on lesion formation. Circ Res. 2002; 90(10):1039-40. DOI: 10.1161/01.res.0000021397.28936.f9. View

3.
von Vietinghoff S, Ley K . Interleukin 17 in vascular inflammation. Cytokine Growth Factor Rev. 2010; 21(6):463-9. PMC: 3005323. DOI: 10.1016/j.cytogfr.2010.10.003. View

4.
Xu F, Ji J, Li L, Chen R, Hu W . Adventitial fibroblasts are activated in the early stages of atherosclerosis in the apolipoprotein E knockout mouse. Biochem Biophys Res Commun. 2006; 352(3):681-8. DOI: 10.1016/j.bbrc.2006.11.073. View

5.
Suh S, Han S, Kim S, Kim H, Chung S, Ryu K . Carotid intima-media thickness and plaque as a predictor for ischemic etiology in patients with severe left ventricular systolic dysfunction. Korean Circ J. 2011; 40(12):665-70. PMC: 3025341. DOI: 10.4070/kcj.2010.40.12.665. View