Downregulation of TIGIT Expression in FOXP3+Regulatory T Cells in Acute Coronary Syndrome

提吉特 FOXP3型 医学 免疫学 流式细胞术 内科学 转化生长因子 调节性T细胞 白细胞介素2受体 内分泌学 T细胞 免疫系统
作者
Xinlin Xiong,Zhenhua Luo,Haiyan Zhou,Zonggang Duan,Li Niu,Kai Zhang,Guangwei Huang,Wei Li
出处
期刊:Journal of Inflammation Research [Dove Medical Press]
卷期号:Volume 15: 1195-1207 被引量:9
标识
DOI:10.2147/jir.s351364
摘要

Little is currently known on the role of T-cell immunoglobulin and ITIM domain (TIGIT) expression in Foxp3+ regulatory T cells (TIGIT+Tregs) in acute coronary syndrome (ACS) patients. The aim of this study was to investigate the role and alterations of TIGIT+Tregs in ACS patients.We enrolled 117 subjects, including 61 ACS patients, 26 chronic coronary syndrome (CCS) patients, and 30 control subjects without coronary artery disease. The quantification of TIGIT+Tregs was determined by flow cytometry; serum interleukin-6 (IL-6) and transforming growth factor-β (TGF-β) were also measured.TIGIT+Tregs expression was significantly lower in ACS patients compared with CCS and control patients (P<0.05). The expression of TIGIT+Tregs was comparable in patients with and without traditional risk factors (P>0.05). Logistic regression analysis revealed that TIGIT+Tregs levels are independent predictors of ACS (P<0.01). Receiver-operating characteristic (ROC) curve analysis showed the expression levels of TIGIT+Tregs had a discriminative power for ACS (P<0.01). IL-6 levels were increased (P<0.01), while TGF-β was decreased in ACS patients compared with CCS and control patients (P<0.01). Meanwhile, an inverse correlation between IL-6 and TIGIT+Tregs was observed (P<0.01), while a positive correlation between TGF-β and TIGIT+Tregs was found (P<0.05).TIGIT+Tregs levels are significantly reduced in ACS, accompanied by upregulated IL-6 and downregulated TGF-β expression. The downregulated TIGIT+Tregs are independent predictors of ACS. These findings suggest that TIGIT+Tregs may have an anti-inflammatory and protective effect on ACS, and its decreased expression may be associated with atherosclerotic plaque destabilization.
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