Author + information
- Caixia Lv1
Atherosclerosis is a chronic inflammatory disease mediated by innate and adaptive immune responses. In recent years, CD4 (+) T cells (Th1, Th2, Treg, and Th17) have been increasingly studied for their role in atherosclerosis pathophysiology, atheroma stability, plaque rupture, and life-threatening acute coronary syndrome. A imbalance between FoxP3+ regulatory T cells (Tregs) and inflammatory T-helper (Th) 17 cells has been suggested, but the result from the previous study was controversial. This study investigated the phenotypical and functional characteristics of Th17 and Tregs and methylation status of RORC/FoxP3 in patients with acute coronary syndrome (ACS).
There was a concurrent accumulation of circulating peripheral Th17 cells and FoxP3+Tregs in patients with ACS. At the transcriptional level, Th17 and Treg-associated transcription factors were elevated in ACS. However, a diminished suppressive function on autologous lymphocytes was found in ACS-derived Tregs. Significant relative hypomethylation was seen at the gene level for RORC1 and RORC2 in ACS, but hypermethylation in FoxP3 gene in ACS.
Besides the high transcriptional activity of T cells, attributed to Treg or Th17 phenotype, in ACS, Tregs may be insufficient to produce high amounts of IL-10 or to control proliferative activity of effector T cells in ACS.
Our results suggest a high plasticity of Tregs strongly associated with the Th17 phenotype. RORC/FoxP3 methylation might be a novel approach to diagnose ACS and to differentiate ACS subtypes.