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

Shu-fang Han1, Peng Liu, Wei Zhang

  • 1Department of Cardiology, Xijing hospital, Fourth Military Medical University, Xi'an, PR China. tangchao@fmmu.edu.cn <tangchao@fmmu.edu.cn>

Clinical Immunology (Orlando, Fla.)
|May 22, 2007
PubMed

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.

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