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The opposite-direction modulation of CD4+CD25+ Tregs and T helper 1 cells in acute coronary syndromes
- Source :
- Clinical Immunology. 124:90-97
- Publication Year :
- 2007
- Publisher :
- Elsevier BV, 2007.
-
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.
- Subjects :
- CD4-Positive T-Lymphocytes
Male
Immunology
Myocardial Infarction
Coronary Disease
chemical and pharmacologic phenomena
Coronary Artery Disease
Angina Pectoris
Angina
Coronary artery disease
Interleukin 21
Th2 Cells
Humans
Immunology and Allergy
Medicine
Angina, Unstable
cardiovascular diseases
IL-2 receptor
Myocardial infarction
Aged
business.industry
Unstable angina
Interleukin-2 Receptor alpha Subunit
FOXP3
Forkhead Transcription Factors
hemic and immune systems
T-Lymphocytes, Helper-Inducer
T lymphocyte
Middle Aged
Th1 Cells
medicine.disease
Gene Expression Regulation
Acute Disease
business
Subjects
Details
- ISSN :
- 15216616
- Volume :
- 124
- Database :
- OpenAIRE
- Journal :
- Clinical Immunology
- Accession number :
- edsair.doi.dedup.....c47b18f4a4c53903818399cef581eb40