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

Clin Immunol. 2007 Jul;124(1):90-7. doi: 10.1016/j.clim.2007.03.546. Epub 2007 May 23.

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.

MeSH terms

  • Acute Disease
  • Aged
  • Angina Pectoris / immunology
  • Angina, Unstable / immunology
  • CD4-Positive T-Lymphocytes / immunology*
  • Coronary Artery Disease / immunology*
  • Coronary Disease / immunology*
  • Forkhead Transcription Factors / immunology*
  • Gene Expression Regulation
  • Humans
  • Interleukin-2 Receptor alpha Subunit / immunology*
  • Male
  • Middle Aged
  • Myocardial Infarction / immunology
  • T-Lymphocytes, Helper-Inducer / immunology
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*

Substances

  • Forkhead Transcription Factors
  • Interleukin-2 Receptor alpha Subunit