Treg/Th17 Imbalance Is Associated With Cardiovascular Complications In Uremic Patients Undergoing Maintenance Hemodialysis

Investigations of Treg/Th17 imbalance associated with cardiovascular complications in hemodialysis are limited. The aim of this study was to examine the association between Treg/Th17 balance and cardiovascular comorbidity in maintenance hemodialysis (MHD). Uremic patients included in the present study were divided into three groups: the WHD group comprising 30 patients with no cardiovascular complications or maintenance hemodialysis (MHD), the MHD1 group comprising 36 patients presenting with cardiovascular complications during MHD, and the MHD2 group comprising 30 patients with a lack of cardiovascular complications during MHD. The control group comprised 20 healthy volunteers. Th17 and Treg cells were measured by fluorescence-activated cell scanning (FACS). IL-6 and IL-10 levels were determined by enzyme-linked immunosorbent assay (ELISA). Monocyte surface expression of the costimulatory molecules CD80 and CD86 was assessed by FACS after the monocytes were cocultured with Th17 or Treg cells in the presence or absence of IL-17. Results revealed that the percentage of Th17 of total CD4(+) cells was significantly higher in the MHD1 (36.27 +/- 9.62% in) and WHD (35.98 +/- 8.85%) groups compared with the MHD2 (19.64 +/- 5.97%) and healthy (1.12 +/- 1.52%) groups. Elevated IL-6 levels were obtained in Th17 cells for the MHD1 and WHD groups, whereas a marked decrease was evident when IL-17 was blocked. However, no significant differences or cardiovascular complications were detected in the expression of CD80 and CD86 in the MHD group, whereas the expression of the uremic subgroups was statistically higher compared with the healthy controls. To the best of our knowledge, this is the first study to demonstrate that the Treg/Th17 imbalance may be associated with the pathogenesis of cardiovascular complications in uremic patients undergoing hemodialysis through the B7-independent upregulation of IL-6 induced by IL-17.