Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study.

IF 1.8 4区 医学 Q3 PERIPHERAL VASCULAR DISEASE Journal of Vascular Research Pub Date : 2024-09-18 DOI:10.1159/000541069
Fernanda Bocanegra-Zamora,Fernanda Espinosa-Bautista,Gian M Jiménez-Rodríguez,Felipe Masso,Araceli Paez,Hector Gonzalez-Pacheco,Mariana Patlán,Guering Eid-Lidt,Luis M Amezcua-Guerra
{"title":"Senescent CD4+ T-Cell Phenotypes and Inflammatory Milieu in the Coronary and Systemic Circulation in ST-Elevation Myocardial Infarction: An Exploratory Study.","authors":"Fernanda Bocanegra-Zamora,Fernanda Espinosa-Bautista,Gian M Jiménez-Rodríguez,Felipe Masso,Araceli Paez,Hector Gonzalez-Pacheco,Mariana Patlán,Guering Eid-Lidt,Luis M Amezcua-Guerra","doi":"10.1159/000541069","DOIUrl":null,"url":null,"abstract":"INTRODUCTION\r\nIn ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear.\r\n\r\nMETHODS\r\nWe examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls.\r\n\r\nRESULTS\r\nOur findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar.\r\n\r\nCONCLUSION\r\nCD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":"9 1","pages":"1-7"},"PeriodicalIF":1.8000,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Vascular Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000541069","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0

Abstract

INTRODUCTION In ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear. METHODS We examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls. RESULTS Our findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275-3,268 vs. 4,278, 3,595-4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar. CONCLUSION CD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
ST段抬高型心肌梗死患者冠状动脉和全身循环中衰老的CD4+ T细胞表型和炎症环境:一项探索性研究
引言 在 ST 段抬高型心肌梗死(STEMI)中,炎症是关键因素,早期衰老的 CD4+CD28null 细胞与心肌梗死的发病机制有关。方法我们检测了 24 名 STEMI 患者冠状窦和腔静脉血液样本中的 CD4+ 细胞亚群,以及 7 名健康对照者的头静脉血液样本。结果我们的研究结果显示,与对照组相比,STEMI 患者的 CD4+ 细胞数量减少(1,998,1,275-3,268 对 4,278,3,595-4,449),同时缺乏 CD28 表达的 CD4+ 细胞比例增加(20.1 对 6.1%)。在 STEMI 中,这些 CD4+CD28 空细胞主要表现出 Th1 表型(47.8% 对 6.6%)。耐人寻味的是,冠状窦和腔静脉中的 CD4+CD28null 细胞没有发现明显差异,而且这些区域的细胞因子水平仍然相似。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Journal of Vascular Research
Journal of Vascular Research 医学-生理学
CiteScore
3.40
自引率
0.00%
发文量
25
审稿时长
>12 weeks
期刊介绍: The ''Journal of Vascular Research'' publishes original articles and reviews of scientific excellence in vascular and microvascular biology, physiology and pathophysiology. The scope of the journal covers a broad spectrum of vascular and lymphatic research, including vascular structure, vascular function, haemodynamics, mechanics, cell signalling, intercellular communication, growth and differentiation. JVR''s ''Vascular Update'' series regularly presents state-of-the-art reviews on hot topics in vascular biology. Manuscript processing times are, consistent with stringent review, kept as short as possible due to electronic submission. All articles are published online first, ensuring rapid publication. The ''Journal of Vascular Research'' is the official journal of the European Society for Microcirculation. A biennial prize is awarded to the authors of the best paper published in the journal over the previous two years, thus encouraging young scientists working in the exciting field of vascular biology to publish their findings.
期刊最新文献
RIP3 augments neuroinflammation by facilitating neutrophil infiltration during an ischemic stroke. Characterising the Time Course of the Dilatory Response of Healthy Retinal Arteries during Flicker-Light Provocation. Perfusion staining methods for visualization of the intact microvascular networks in whole mount skeletal muscle preparations. Cerebral Cortical Vasodilation via Nicotinic Receptors by Heated Tobacco Product Aerosol Extract in Rats. Rivaroxaban as a protector of Oxidative Stress-induced Vascular Endothelial Glycocalyx Damage via The IQGAP1/PAR1-2/PI3K/Akt Pathway.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1