Regulatory T-cell frequency and function in acute myocardial infarction patients and its correlation with ventricular dysfunction.

IF 3.8 3区 医学 Q3 IMMUNOLOGY Clinical and experimental immunology Pub Date : 2024-05-16 DOI:10.1093/cei/uxae014
Elena Berenice Martínez-Shio, Laura Sherell Marín-Jáuregui, Alma Celeste Rodríguez-Ortega, Lesly Marsol Doníz-Padilla, Roberto González-Amaro, Carlos David Escobedo-Uribe, Adriana Elizabeth Monsiváis-Urenda
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Abstract

A high percentage of patients with acute coronary syndrome develop heart failure due to the ischemic event. Regulatory T (Treg) cells are lymphocytes with suppressive capacity that control the immune response and include the conventional CD4+ CD25hi Foxp3+ cells and the CD4+ CD25var CD69+ LAP+ Foxp3- IL-10+ cells. No human follow-up studies focus on Treg cells' behavior after infarction and their possible relationship with ventricular function as a sign of postischemic cardiac remodeling. This study aimed to analyze, by flow cytometry, the circulating levels of CD69+ Treg cells and CD4+ CD25hi Foxp3+ cells, their IL-10+ production as well as their function in patients with acute myocardial infarction (AMI), and its possible relation with ventricular dysfunction. We found a significant difference in the percentage of CD4+ CD25hi Foxp3+ cells and IL-10+ MFI in patients with AMI at 72 hours compared with the healthy control group, and the levels of these cells were reduced 6 months post-AMI. Regarding the suppressive function of CD4+ CD25+ regulatory cells, they were dysfunctional at 3 and 6 months post-AMI. The frequency of CD69+ Treg cells was similar between patients with AMI at 72 hours postinfarction and the control groups. Moreover, the frequency of CD69+ Treg cells at 3 and 6 months postischemic event did not vary over time. Treg cells play a role in regulating inflammation after an AMI, and its function may be compromised in this pathology. This work is the first report to evaluate CD69+ Foxp3- Treg cells in AMI patients.

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急性心肌梗死患者调节性 T 细胞的频率和功能及其与心室功能障碍的相关性。
急性冠状动脉综合征患者中有很大一部分会因缺血事件而导致心力衰竭。调节性 T(Treg)细胞是具有抑制能力的淋巴细胞,可控制免疫反应,包括传统的 CD4+ CD25hi Foxp3+ 细胞和 CD4+ CD25var CD69+ LAP+ Foxp3- IL-10+ 细胞。目前还没有人类跟踪研究关注 Treg 细胞在心肌梗塞后的行为及其与心室功能的可能关系(作为缺血后心脏重塑的标志)。本研究旨在通过流式细胞术分析急性心肌梗死(AMI)患者循环中 CD69+ 调节性 T 细胞和 CD4+ CD25hi Foxp3+ 细胞的水平、IL-10+ 的产生及其功能,以及它们与心室功能障碍的可能关系。我们发现,与健康对照组相比,急性心肌梗死患者在 72 小时内的 CD4+ CD25hi Foxp3+ 细胞百分比和 IL-10+ MFI 有明显差异,而且这些细胞的水平在急性心肌梗死后 6 个月有所降低。至于 CD4+ CD25+ 调节细胞的抑制功能,它们在急性心肌梗死后 3 个月和 6 个月时功能失调。急性心肌梗死患者在梗死后 72 小时内的 CD69+ Treg 细胞频率与对照组相似。此外,缺血事件后三个月和六个月时,CD69+ Treg 细胞的频率并不随时间变化。Treg 细胞在急性心肌梗死后的炎症调节中发挥作用,其功能可能在这种病理情况下受到损害。这项研究首次对急性心肌梗死患者的 CD69+ Foxp3- Treg 细胞进行了评估。
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来源期刊
CiteScore
8.40
自引率
2.20%
发文量
101
审稿时长
3-8 weeks
期刊介绍: Clinical & Experimental Immunology (established in 1966) is an authoritative international journal publishing high-quality research studies in translational and clinical immunology that have the potential to transform our understanding of the immunopathology of human disease and/or change clinical practice. The journal is focused on translational and clinical immunology and is among the foremost journals in this field, attracting high-quality papers from across the world. Translation is viewed as a process of applying ideas, insights and discoveries generated through scientific studies to the treatment, prevention or diagnosis of human disease. Clinical immunology has evolved as a field to encompass the application of state-of-the-art technologies such as next-generation sequencing, metagenomics and high-dimensional phenotyping to understand mechanisms that govern the outcomes of clinical trials.
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