IF 4.6 2区 医学 Q2 IMMUNOLOGY
Jiafu Wang, Song Li, Xianling Zhou, Hongxing Wu, Xiaolan Ouyang, Zhuoshan Huang, Long Peng, Qian Chen, Yuman Wu, Zhitong Li, Ziyi Peng, Yi Yang, Yan Lu, Xixiang Tang, Yue Li, Suhua Li
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引用次数: 0

摘要

目的 心肌缺血和重塑是导致冠状动脉疾病(CAD)恶化和死亡的主要原因。以前的研究显示,CAD 患者的免疫细胞发生了变化,但其特征及其与心肌缺血和重塑的关系仍不清楚。 方法 我们比较了无 CAD 患者、CAD 患者和 CAD 合并心力衰竭(HF)患者的免疫细胞变化。 结果 我们发现,在三个患者组中,循环中的粘膜相关不变 T 细胞(MAIT)逐渐减少。MAIT 细胞的活化标志物(CD69 和 PD-1)和细胞毒性分子(如颗粒酶 B)表达增加。MAIT 细胞的特征与心肌缺血和重塑的临床指标恶化呈正相关,包括 Gensini 评分、cTnI、NT-proBNP、LVEF 和 E/e′。此外,MAIT 细胞的减少、活化和细胞毒性与心肌纤维化指标(sST2、Gal-3、PICP 和 PIIINP)有关,这是心肌重塑的核心病理机制。最后,我们初步探讨了导致 CAD 患者 MAIT 细胞异常的潜在诱因,发现肠道屏障功能受损和循环细菌抗原增加可能是导致这些变化的原因。 结论 在 CAD 进展过程中,我们观察到循环 MAIT 细胞减少。MAIT 细胞的活化和细胞毒性增强与心力衰竭的 CAD 患者心肌缺血和重塑有关,这可能是由肠道微生物渗漏引发的。我们的研究结果为监测和干预疾病进展提供了一种新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mucosal-associated invariant T cells correlate with myocardial ischaemia and remodelling in coronary artery disease

Mucosal-associated invariant T cells correlate with myocardial ischaemia and remodelling in coronary artery disease

Objectives

Myocardial ischaemia and remodelling are major contributors to the progression and mortality of coronary artery disease (CAD). Previous studies have shown immune cell alterations in CAD patients, but their characteristics and associations with myocardial ischaemia and remodelling remain unclear.

Methods

We compared immune cell changes among patients without CAD, those with CAD and those with CAD and heart failure (HF).

Results

We found a progressive reduction in circulating mucosal-associated invariant T (MAIT) cells across the three patient groups. MAIT cells exhibited increased expression of activation markers (CD69 and PD-1) and cytotoxic molecules (such as granzyme B). The features of MAIT cells were correlated positively with worsening clinical indicators of myocardial ischaemia and remodelling, including the Gensini score, cTnI, NT-proBNP, LVEF and E/e′. Additionally, the reduction, activation and cytotoxicity of MAIT cells were associated with indicators of myocardial fibrosis (sST2, Gal-3, PICP and PIIINP), a central pathological mechanism of myocardial remodelling. Finally, we preliminarily explored potential triggers for MAIT cell abnormalities in CAD patients and found that impaired intestinal barrier function and increased circulating bacterial antigens may contribute to these changes.

Conclusions

During CAD progression, we observed a decrease in circulating MAIT cells. Enhanced activation and cytotoxicity of MAIT cells are associated with myocardial ischaemia and remodelling in CAD patients with heart failure, potentially triggered by gut microbial leakage. Our findings suggest a novel strategy for monitoring and intervention in disease progression.

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来源期刊
Clinical & Translational Immunology
Clinical & Translational Immunology Medicine-Immunology and Allergy
CiteScore
12.00
自引率
1.70%
发文量
77
审稿时长
13 weeks
期刊介绍: Clinical & Translational Immunology is an open access, fully peer-reviewed journal devoted to publishing cutting-edge advances in biomedical research for scientists and physicians. The Journal covers fields including cancer biology, cardiovascular research, gene therapy, immunology, vaccine development and disease pathogenesis and therapy at the earliest phases of investigation.
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