Accumulating evidence suggests that abnormal inflammation plays a critical role in the pathogenesis of pulmonary arterial hypertension (PAH). CD8CD25Foxp3 T cell is a novel cell subtype， and its role in PAH is not yet investigated. Here， we observed that PAH patients presented a significant upregulation of CD8CD25Foxp3 T cells and a downregulation of CD4CD25Foxp3 T cells compared to healthy controls. Regardless， the total number of CD25Foxp3 T cells in PAH patients was still smaller than that in healthy controls. Compared to CD8CD25 T cells， CD8CD25 T cells presented higher Foxp3 expression， lower interferon (IFN)-γ expression and higher transforming growth factor (TGF)-β expression， in both healthy and PAH individuals. The CD8CD25 T cells in PAH patients also demonstrated regulatory function by suppressing the proliferation of CD4CD25 and CD8CD25 effector T cells， albeit at lower efficiency than CD4CD25 T cells from PAH patients and healthy volunteers. CD8CD25 T cells from PAH responded to interleukin (IL)-2 supplement by expansion and upregulating Foxp3 expression. In PAH patients， IL-2-treated CD8CD25 T cells were more potent at inhibiting CD4CD25 effector T cell proliferation than IL-2-untreated CD8CD25 T cells. Together， we found an upregulation of CD8CD25Foxp3 T cells in PAH patients， and this T cell population presented suppressive activity that could be enhanced by IL-2 treatment.