Abstract

T helper 17 (Th17) and regulatory T (Treg) cells play an important role in pathogenesis of systemic lupus erythematosus (SLE). Their imbalance was reported in treated SLE patients, while very little is known about the relationship between Th17 and Treg cells in new-onset untreated SLE patients. To assess the role of Th17/Treg cells in the pathogenesis of new-onset SLE. Thirty-nine new-onset SLE patients and 33 age-matched healthy adults were enrolled. We analysed Th17 and Treg cells in different level, including their frequencies in peripheral blood mononuclear cell, the expression of interleukin-17 A (IL-17A) and forkhead box P3 (FoxP3) proteins, the expression of retinoid-related orphan nuclear receptor γt (RORγt) and FoxP3 genes and plasma level of IL-17A. The frequency of Th17 and Treg cells, the expression of IL-17A among Th17 cell, the plasma level of IL-17A, the expression of RORγt and FoxP3 genes were all significantly higher in SLE patients. Th17 cells were negatively correlated with Treg cells. We also found that plasma level of IL-17A was positively correlated with SLE disease activities index (SLEDAI) scores and an equation among the level of C3, IgA, IL-17A and SLEDAI scores. Results indicate that Th17 and Treg cells take roles in the pathogenesis of SLE. Th17 cells might suppress the differentiation of Treg cells, and feedback effects might exist between them during SLE pathogenesis. The measure of plasma level of IL-17A may be useful for evaluation of disease activity in new-onset SLE patients.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call