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Low responder T cell susceptibility to the suppressive function of regulatory T cells in patients with dilated cardiomyopathy
  1. Hongxia Tang1,a,
  2. Yucheng Zhong1,a,
  3. Yuntao Zhu1,
  4. Fang Zhao2,
  5. Xiaoxue Cui1,
  6. Zhaohui Wang1
  1. 1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
  2. 2Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, China
  1. Correspondence to Professor Zhaohui Wang, Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jie-Fang Avenue, Wuhan, 430022, China; sgwangtjm{at}163.com

Abstract

Objective The pathogenesis of dilated cardiomyopathy (DCM) is closely connected with dysfunction of the autoimmune system, and CD4+CD25highCD127low/− regulatory T (Treg) cells have a vital role in maintaining self-tolerance. In this study, we compared the frequency and regulatory function of Treg cells between DCM patients and normal controls.

Methods and Results The frequencies of CD4+CD25+ T cells in DCM patients were statistically decreased compared with normal controls (p<0.05) by flow cytometry, and the levels of FOXP3 mRNA and protein expression in PBMCs (peripheral blood mononuclear cells) of DCM patients were lower than those of normal controls (p<0.01), using real-time RT-PCR assay and western blot. Notably, the suppressive capacity of CD4+CD25highCD127low/− regulatory T cells of DCM patients acting on autologous CD4+CD25 responder T (Tresp) cells seemed to be partially impaired (43.83±3.19% suppression versus 63.17±3.66% in normal controls, p=0.01). Surprisingly, Treg cells from DCM patients efficiently suppressed the proliferation of Tresp cells from normal subjects to the similar level as Treg cells from normal subjects on autologous Tresp cells (p=0.286), whereas Treg cells of normal subjects poorly inhibited the proliferation of Tresp cells from DCM patients.

Conclusion The defective capacity of Treg cells suppressing autologous Tresp cells is attributed to the increasing resistance of Tresp cells to inhibition of Treg cells in DCM patients. Therefore, strategies to improve the susceptibility of Tresp cells to Treg cell-mediated suppression might benefit DCM patients.

  • T-lymphocytes, regulatory
  • responder T cell
  • cardiomyopathy, dilated
  • FOXP3 protein, human
  • suppressive function

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Footnotes

  • a These authors contributed equally to this work.

  • Funding National Basic Research Program of China (973 Program)£°2007CB512000£»2007CB512005.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the Ethics Committee of Tongji Medical College of Huazhong University of Science and Technology.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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