Recruitment of myeloid-derived suppressor cells and regulatory T-cells is associated with the occurrence of acute myocardial infarction

被引:5
|
作者
Zhang, Mingqiang [1 ]
Shi, Xiaohu [2 ]
Zhao, Jingquan [1 ]
Guo, Wenjia [1 ]
Zhou, Jie [3 ]
机构
[1] Tsinghua Univ, Beijing Tsinghua Changgung Hosp, Sch Clin Med, Dept Resp & Crit Care Med, Beijing 102218, Peoples R China
[2] Peking Union Med Coll & Chinese Acad Med Sci, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China
[3] Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Cardiol, 32 Yihuan Rd, Chengdu 610072, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
acute myocardial infarction; myeloid-derived suppressor cells; regulatory T-cells; granulocytic phenotype; monocytic phenotype; INFLAMMATION; PD-L1; MICROENVIRONMENT; ACCUMULATION; INJURY;
D O I
10.3892/br.2023.1637
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The roles of myeloid-derived suppressor cells (MDSCs) and regulatory T-cells (Tregs) in acute myocardial infarction (AMI) remain elusive. The present study aimed to analyze the proportions of the granulocytic and monocytic populations of MDSCs (G-MDSCs and M-MDSCs, respectively), and Tregs in the peripheral blood mononuclear cells (PBMCs) of patients with AMI. The present study recruited 34 patients with AMI and 37 healthy controls without clinical signs of myocardial ischemia. PBMCs were isolated from the peripheral blood samples of patients with AMI within 24 h following admission to the hospital and from those of the healthy controls during a physical examination. Two subsets of MDSCs, G-MDSCs (CD15(+)CD33(+)CD11b(+)CD14(-)HLA-DRlow) and M-MDSCs (CD14(+)CD15(-)CD11b(+)HLA-DRlow), and Tregs (CD3(+)CD4(+)CD25(high)CD127(low) T-cells) in the PBMCs derived from the patients with AMI and healthy controls were analyzed using flow cytometry. The effects of MDSCs derived from patients with AMI on naive CD4(+) T-cells were examined in the co-culture system. The results revealed that the proportions of G-MDSCs and M-MDSCs were higher in the peripheral blood of patients with AMI than in that of the healthy controls. The patients with AMI had significantly higher numbers of programmed death-ligand (PD-L)1- and PD-L2-positive G-MDSCs and M-MDSCs compared with the healthy controls (P<0.05). The MDSCs could acquire a granulocytic phenotype following AMI, and the G-MDSCs and M-MDSCs would be more likely to express PD-L2 and PD-L1, respectively. The ratios of Tregs to CD4(+) T-cells and PD-1(+) Tregs in the peripheral blood of patients with AMI were significantly higher than those in the healthy controls (P<0.05). The results of flow cytometry demonstrated an increase in the numbers of inducible Tregs in the co-culture system with the G-MDSCs derived from patients with AMI compared with the G-MDSCs derived from the healthy controls (P<0.01). On the whole, the findings presented herein demonstrate the accumulation of MDSCs, and the upregulation of PD-L1 and PD-L2 expression on the surface of MDSCs in patients with AMI. MDSCs can induce the expansion of Tregs by binding PD-1 on the surface of Tregs, thus playing a crucial role in AMI.
引用
收藏
页数:14
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