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.

Immunology
|February 17, 2017
PubMed

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.

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