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10.1111/cei.12897

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suck abstract from ncbi


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pmid27997991
      Clin+Exp+Immunol 2017 ; 187 (3 ): 441-454
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  • Decreased frequencies and impaired functions of the CD31(+) subpopulation in T(reg) cells associated with decreased FoxP3 expression and enhanced T(reg) cell defects in patients with coronary heart disease #MMPMID27997991
  • Huang L ; Zheng Y ; Yuan X ; Ma Y ; Xie G ; Wang W ; Chen H ; Shen L
  • Clin Exp Immunol 2017[Mar]; 187 (3 ): 441-454 PMID27997991 show ga
  • Coronary heart disease (CHD) is one of the most common types of organ lesions caused by atherosclerosis, in which CD4(+) CD25(+) forkhead box protein 3 (FoxP3(+) ) regulatory T cells (T(reg) ) play an atheroprotective role. However, T(reg) cell numbers are decreased and their functions are impaired in atherosclerosis; the underlying mechanisms remain unclear. CD31 plays an important part in T cell response and contributes to maintaining T cell tolerance. The immunomodulatory effects of CD31 are also implicated in atherosclerosis. In this study, we found that decreased frequencies of the CD31(+) subpopulation in T(reg) cells (CD31(+) Tr cells) correlated positively with decreased FoxP3 expression in CHD patients. Cell culture in vitro demonstrated CD31(+) Tr cells maintaining stable FoxP3 expression after activation and exhibited enhanced proliferation and immunosuppression compared with the CD31(-) subpopulation in T(reg) cells (CD31(-) Tr cells). We also confirmed impaired secretion of transforming growth factor (TGF)-?1 and interleukin (IL)-10 in CD31(+) Tr cells of CHD patients. Further analysis revealed reduced phospho-SHP2 (associated with CD31 activation) and phospho-signal transducer and activator of transcription-5 (STAT-5) (associated with FoxP3 transcription) levels in CD31(+) Tr cells of CHD patients, suggesting that decreased FoxP3 expression in CD31(+) Tr cells might be because of attenuated SHP2 and STAT-5 activation. These data indicate that decreased frequencies and impaired functions of the CD31(+) Tr subpopulation associated with decreased FoxP3 expression give rise, at least in part, to T(reg) cell defects in CHD patients. Our findings emphasize the important role of the CD31(+) Tr subpopulation in maintaining T(reg) cell normal function and may provide a novel explanation for impaired immunoregulation of T(reg) cells in CHD.
  • |Cells, Cultured [MESH]
  • |Coronary Artery Disease/*immunology/metabolism [MESH]
  • |Female [MESH]
  • |Forkhead Transcription Factors/*metabolism [MESH]
  • |Humans [MESH]
  • |Immune Tolerance/immunology [MESH]
  • |Interleukin-10/metabolism [MESH]
  • |Leukocytes, Mononuclear/immunology/metabolism [MESH]
  • |Male [MESH]
  • |Middle Aged [MESH]
  • |Platelet Endothelial Cell Adhesion Molecule-1/*metabolism [MESH]
  • |Protein Tyrosine Phosphatase, Non-Receptor Type 11/metabolism [MESH]
  • |STAT5 Transcription Factor/metabolism [MESH]
  • |T-Lymphocytes, Regulatory/*immunology/metabolism [MESH]


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