title: The opposite-direction modulation of CD4+CD25+ Tregs and T helper 1 cells in acute coronary syndromes.
abstract: 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.
authors.affiliation: Department of Cardiology, Xijing hospital, Fourth Military Medical University, Xi'an, PR China. tangchao@fmmu.edu.cn <tangchao@fmmu.edu.cn>
authors.forename: Shu-fang
authors.initials: SF
authors.lastname: Han
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Lun
authors.initials: L
authors.lastname: Bu
authors.forename: Min
authors.initials: M
authors.lastname: Shen
authors.forename: Hu
authors.initials: H
authors.lastname: Li
authors.forename: Yan-hong
authors.initials: YH
authors.lastname: Fan
authors.forename: Kang
authors.initials: K
authors.lastname: Cheng
authors.forename: He-xiang
authors.initials: HX
authors.lastname: Cheng
authors.forename: Cheng-xiang
authors.initials: CX
authors.lastname: Li
authors.forename: Guo-liang
authors.initials: GL
authors.lastname: Jia
mesh_terms: D000208:Acute Disease; D000368:Aged; D000787:Angina Pectoris / Q000276:immunology; D000789:Angina, Unstable / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003324:Coronary Artery Disease / Q000276:immunology*; D003327:Coronary Disease / Q000276:immunology*; D051858:Forkhead Transcription Factors / Q000276:immunology*; D005786:Gene Expression Regulation; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D051858:Forkhead Transcription Factors; D053645:Interleukin-2 Receptor alpha Subunit