The opposite-direction modulation of CD4+CD25+ Tregs and T helper 1 cells in acute coronary syndromes

Different subsets of T lymphocytes have different functions in atherosclerosis advancement. T helper 1 cells and T regulatory 1 cells have been demonstrated to play opposite roles in rupture of atherosclerotic lesion. However, the role of novel subset of T regulatory cells, known as CD4+CD25+Foxp3+...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 124(2007), 1 vom: 31. Juli, Seite 90-7
1. Verfasser: Han, Shu-fang (VerfasserIn)
Weitere Verfasser: Liu, Peng, Zhang, Wei, Bu, Lun, Shen, Min, Li, Hu, Fan, Yan-hong, Cheng, Kang, Cheng, He-xiang, Li, Cheng-xiang, Jia, Guo-liang
Format: Aufsatz
Sprache:English
Veröffentlicht: 2007
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Forkhead Transcription Factors Interleukin-2 Receptor alpha Subunit
Beschreibung
Zusammenfassung:Different subsets of T lymphocytes have different functions in atherosclerosis advancement. T helper 1 cells and T regulatory 1 cells have been demonstrated to play opposite roles in rupture of atherosclerotic lesion. However, the role of novel subset of T regulatory cells, known as CD4+CD25+Foxp3+ T cells, remains largely unknown in coronary artery disease (CAD). In this study, we investigated the peripheral CD4+CD25+Foxp3+ T cells of patients with CAD and controls. The patients submitted were divided into three groups: stable angina pectoris (SA) group, unstable angina pectoris (UA) group and acute myocardial infarction (AMI) group. We analyzed the frequencies of peripheral CD4+CD25+Foxp3+ T cells and T helper 1/T helper 2 cells, expression of Foxp3 in CD4+CD25+ T subsets and cytokines pattern in patients and controls. We found that the reduction of CD4+CD25+Foxp3+ T lymphocytes was consistent with the expansion of Th1 cells in patients with unstable CAD. The reversed development between CD4+CD25+ Tregs and Th1 cells might contribute to plaque destabilization
Beschreibung:Date Completed 10.08.2007
Date Revised 08.04.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035