Related Experiment Video
Updated: Mar 7, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
CD4+ CD25+ GARP+ regulatory T cells display a compromised suppressive function in patients with dilated
Yuzhen Wei1, Kunwu Yu1, Hui Wei2
1Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, TongJi Medical College, Huahzong University of Science and Technology, Wuhan, China.
Insights
Dilated cardiomyopathy (DCM) involves immune system dysfunction. This study found that regulatory T cells expressing GARP (Glycoprotein A repetitions predominant) are reduced and less effective in DCM patients, suggesting GARP
Area of Science:
- Immunology
- Cardiology
- Molecular Biology
Background:
- Dilated cardiomyopathy (DCM) is an inflammatory heart condition linked to immune system dysfunction.
- Glycoprotein A repetitions predominant (GARP) is expressed on regulatory T cells (Tregs) and mediates suppressive activity.
Purpose of the Study:
- To investigate the frequency and function of circulating CD4+ CD25+ GARP+ regulatory T cells in DCM patients.
- To explore the role of GARP as a molecular marker for regulatory T cell phenotype in DCM.
Main Methods:
- Comparative analysis of immune cell populations (Tregs, Th1, Th17) and cytokine levels (IFN-γ, IL-17, TGF-β1) in DCM patients and healthy controls.
- Assessment of regulatory T cell suppressive function using CFSE dye assay.
- Measurement of cytokine production by cultured regulatory T cells via ELISA.
Main Results:
- DCM patients exhibited increased Th1 and Th17 cells with elevated IFN-γ and IL-17 levels.
- A significant decrease in Treg cell numbers, TGF-β1 levels, and FOXP3/GARP expression was observed in DCM patients.
- Impaired suppressive function of CD4+ CD25+ GARP+ Treg cells was detected in DCM patients.
- Cultured Tregs from DCM patients produced lower TGF-β1 and higher IFN-γ and IL-17.
Conclusions:
- Circulating CD4+ CD25+ GARP+ regulatory T cells are functionally deficient in DCM.
- GARP may serve as a more precise molecular marker for the regulatory T cell phenotype in DCM.
- Targeting GARP could be a potential therapeutic strategy for DCM.
Abstract:
Dilated cardiomyopathy (DCM) is a lethal inflammatory heart disease and closely connected with dysfunction of the immune system. Glycoprotein A repetitions predominant (GARP) expressed on activated CD4+ T cells with suppressive activity has been established. This study aimed to investigate the frequency and function of circulating CD4+ CD25+ GARP+ regulatory T (Treg) cells in DCM. Forty-five DCM patients and 46 controls were enrolled in this study. There was a significant increase in peripheral T helper type 1 (Th1) and Th17 number and their related cytokines [interferon-γ (IFN-γ), interleukin (IL-17)], and an obvious decrease in Treg number, transforming growth factor-β1 (TGF-β1 ) levels and the expression of forkhead box P3 (FOXP3) and GARP in patients with DCM compared with controls. In addition, the suppressive function of CD4+ CD25+ GARP+ Treg cells was impaired in DCM patients upon T-cell receptor stimulation detected using CFSE dye. Lower level of TGF-β1 and higher levels of IFN-γ and IL-17 detected using ELISA were found in supernatants of the cultured CD4+ CD25+ GARP+ Treg cells in DCM patients compared with controls. Together, our results indicate that CD4+ CD25+ GARP+ Treg cells are defective in DCM patients and GARP seems to be a better molecular definition of the regulatory phenotype. Therefore, it might be an attractive stategy to pay more attention to GARP in DCM patients.
Related Concept Videos
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy V: Interprofessional Care
Imbalances in Cardiac Output
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...
Cardiomyopathy I: Introduction and Classification

