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Downregulation of T helper cell type 3 in patients with acute coronary syndrome
Qing-wei Ji1, Min Guo, Jin-song Zheng
1Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Insights
Decreased T helper 3 (Th3) cells and TGF-beta1 levels are linked to acute coronary syndrome (ACS). This suggests Th3 cells may influence plaque instability and ACS onset in patients.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Atherosclerosis Research
Background:
- Th1/Th2 imbalance is implicated in atherosclerosis and acute coronary syndrome (ACS).
- T helper 3 (Th3) cells secrete TGF-beta1 and can inhibit Th1/Th2 responses.
- The role of Th3 cells in plaque destabilization and ACS onset requires investigation.
Purpose of the Study:
- To investigate the involvement of Th3 cells in plaque destabilization.
- To determine the association between Th3 cells and the onset of acute coronary syndrome (ACS).
Main Methods:
- Ninety-one patients undergoing diagnostic catheterization were grouped: AMI, unstable angina, stable angina, and chest pain syndrome.
- Flow cytometry was used to quantify Th1, Th2, and Th3 cell frequencies.
- ELISA measured concentrations of IFN-gamma, IL-4, and TGF-beta1.
Main Results:
- Patients with ACS showed a significant decrease in peripheral Th3 cell numbers compared to stable angina and chest pain syndrome groups (p<0.01).
- Lower levels of TGF-beta1 were observed in ACS patients versus stable angina and chest pain syndrome groups (p<0.01).
- An imbalance between Th1 and Th2 cells was also noted in ACS patients.
Conclusions:
- Downregulation of Th3 cells may contribute to plaque destabilization.
- Reduced Th3 cell activity is potentially involved in the pathogenesis of ACS.
- Th3 cells represent a potential therapeutic target for managing ACS.
Background And Aims:
There is an imbalance between Th1 and Th2 in the development and progression of atherosclerosis and in patients with acute coronary syndrome (ACS) including acute myocardial infarction (AMI) and unstable angina. T helper cell type 3 (Th3), which primarily secretes transforming growth factor beta-1 (TGF-beta1), has been shown to inhibit both Th1 and Th2 cells. The present study was designed to investigate whether Th3 cells are involved in plaque destabilization and the onset of ACS.
Methods:
Ninety one patients who underwent diagnostic catheterization were classified into four groups (AMI group, unstable angina group, stable angina group and chest pain syndrome group). The cell frequencies of Th1, Th2 and Th3 were detected using flow cytometry, and the concentrations of their related cytokines IFN-gamma, IL-4 and TGF-beta1 were studied by ELISA.
Results:
Apart from the imbalance between Th1 and Th2, results revealed a significant decrease in peripheral Th3 number and levels of TGF-beta1 in patients with ACS as compared with those in patients with stable angina and chest pain syndrome (p<0.01).
Conclusions:
Downregulation of Th3 cells in patients with ACS may play a potential role in plaque destabilization and the onset of ACS.
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