Key result
Chronic heart failure was associated with a significantly lower frequency of naive regulatory T cells (0.59% vs 1.17%) and increased spontaneous apoptosis compared to non-CHF controls.
Case-Control (n=95)
No
Treg-cell defects in chronic heart failure patients are likely driven by decreased thymic output of nascent Treg cells and increased susceptibility to peripheral apoptosis.
Answers are grounded in this paper and cite their sources.
Treg defects may reflect immune dysregulation in CHF; hypothesis-generating for immunomodulation, requires prospective validation.
OBJECTIVE: Animal studies suggest that regulatory T (T(reg)) cells play a beneficial role in ventricular remodeling and our previous data have demonstrated defects of T(reg) cells in patients with chronic heart failure (CHF). However, the mechanisms behind T(reg-)cell defects remained unknown. We here sought to elucidate the mechanism of T(reg-)cell defects in CHF patients. METHODS AND RESULTS: We performed flow cytometry analysis and demonstrated reduced numbers of peripheral blood CD4(+)CD25(+)FOXP3(+)CD45RO(-)CD45RA(+) naïve T(reg) (nT(reg)) cells and CD4(+)CD25(+)FOXP3(+)CD45RO(+)CD45RA(-) memory T(reg) (mT(reg)) cells in CHF patients as compared with non-CHF controls. Moreover, the nT(reg)/mT(reg) ratio (p<0.01), CD4(+)CD25(+)FOXP3(+)CD45RO(-) CD45RA(+)CD31(+) recent thymic emigrant T(reg) cell (RTE-T(reg)) frequency (p<0.01), and T-cell receptor excision circle levels in T(reg) cells (p<0.01) were lower in CHF patients than in non-CHF controls. Combined annexin-V and 7-AAD staining showed that peripheral T(reg) cells from CHF patients exhibited increased spontaneous apoptosis and were more prone to interleukin (IL)-2 deprivation- and CD95 ligand-mediated apoptosis than those from non-CHF individuals. Furthermore, analyses by both flow cytometry and real-time polymerase chain reaction showed that T(reg)-cell frequency in the mediastinal lymph nodes or Foxp3 expression in hearts of CHF patients was no higher than that of the non-CHF controls. CONCLUSION: Our data suggested that the T(reg)-cell defects of CHF patients were likely caused by decreased thymic output of nascent T(reg) cells and increased susceptibility to apoptosis in the periphery.
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Tang et al. (2011) conducted a case-control in Chronic Heart Failure (n=95). Chronic Heart Failure vs. Non-CHF controls was evaluated on Naive regulatory T cell (nTreg) frequency within CD4+ T cells (p=<0.01). Chronic heart failure was associated with a significantly lower frequency of naive regulatory T cells (0.59% vs 1.17%) and increased spontaneous apoptosis compared to non-CHF controls.
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