Rheumatoid arthritis (RA) is a common autoimmune disease, which is usually treated with a combination of anti-rheumatic drugs. However, the clinical remission rate only reaches 40–57% despite serious side effects[
1]. Recently, mesenchymal stem cell (MSC) transplantation has provided an alternative choice for treatment of autoimmune diseases. Animal model studies have found that MSC transplantation significantly improves the autoimmune cerebrospinal meningitis, multiple sclerosis, glomerulonephritis, systemic lupus erythematosus and other autoimmune diseases[
2‐
5]. Although the mechanism remains largely unknown, MSCs have been shown to play a role in differentiation and proliferation of T lymphocytes[
6,
7]. Recent studies have found that RA patients with joint inflammation have increased helper T lymphocyte cells (Th1) and IL-17 cytokine producing T lymphocytes, which lead to a high level of IL-17 in synovial fluid[
8]. Besides IL-17A and IL-17F, Th17 cells also express IL-6, TNF, IL-21 and IL-26. Results from a collagen-induced arthritis (CIA) animal model indicate that IL-17 receptor signalling is a critical inflammatory regulator[
8,
9]. Thus, overexpression of IL-17 may be associated with the pathogenesis of RA. Orphan nuclear receptor gamma (ROR-γ) is a key transcription factor for the differentiation of Th17 cells and regulates IL-17 expression
in vivo and
in vitro. ROR-γ knockout mice have shown reduction of Th17 cells and decreased incidence of autoimmune diseases[
10]. Therefore, investigating the interaction between MSCs and Th17 may help to understand the immunological regulation and pathogenesis of RA. In this study, we designed an
in vitro co-culture system to observe the immunoregulatory effect of MSCs on Th17 cells of RA patients.