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Impairment of Circulating CD4+CD25+GARP+ Regulatory T Cells in Patients with Acute Coronary Syndrome

Authors :
Yucheng Zhong
Wei Zhang
Bangwei Wu
Mingjian Lang
Yingzhong Lin
Xiaobo Mao
Qingwei Ji
Kunwu Yu
Xiaoqi Zhao
Zhengfeng Zhu
Yudong Peng
Yuzhou Liu
Qiutang Zeng
Kai Meng
Ying Huang
Source :
Cellular Physiology and Biochemistry, Vol 33, Iss 3, Pp 621-632 (2014)
Publication Year :
2014
Publisher :
Cell Physiol Biochem Press GmbH & Co KG, 2014.

Abstract

Background: Atherosclerosis (AS) is an inflammatory and immune disease. Regulatory T cells (Tregs) suppress the activation of T cells and have been shown to play a protective role during the pathogenesis of AS. However, specific markers for Tregs are lacking. Recently, glycoprotein A repetitions predominant (GARP) was discovered as a specific marker of activated Tregs, and we therefore utilized GARP as a specific surface marker for Tregs in the current study. Methods: To assess whether GARP+ Tregs are downregulated in patients with acute coronary syndrome (ACS), we examined CD4+CD25+GARP+ T cell frequencies as well as their associated cytokines and suppressive function. Additionally, we compared GARP expression to that of FOXP3, which may be more sensitive as a marker of activated Tregs in patients with ACS. Results: Patients with ACS demonstrated a significant decrease in circulating CD4+CD25+GARP+ Tregs. Moreover, the suppressive function of Tregs and levels of related cytokines were also impaired in ACS patients compared to those with stable angina (SA) or normal coronary artery (NCA). Additionally, after TCR stimulation, peripheral blood mononuclear cells (PBMCs) from patients with ACS exhibited a decrease in CD4+CD25+GARP+ Tregs. Conclusions: These fnding indicate that circulating CD4+CD25+GARP+ Tregs are impaired in patients withACS. Thus, targeting GARP may promote the protective function of Tregs in ACS.

Details

Language :
English
ISSN :
14219778 and 10158987
Volume :
33
Issue :
3
Database :
OpenAIRE
Journal :
Cellular Physiology and Biochemistry
Accession number :
edsair.doi.dedup.....8a71479f9b25d1b3971f236ef2684940