Recently, RA is described as an autoimmune disease mediated by T cells, especially effector the T helper 17 cells (Th17 cells) [1]. The protective role of T regulatory cells (Treg cells) and the pro-inflammatory role of Th17 (by secreting IL-17) have been elucidated and emphasized in the pathogenesis of RA. In patients with active RA increased Th17 levels and decreased Treg levels were found. Th17 and Treg cells (Th17/Treg balance) have a fundamental role in determining the outcome of RA.

Th17 cells play an important role in maintaining mucosal barriers and contributing to pathogen clearance at mucosal surfaces. In the case of autoimmune disorders, Th17 cell over activation can cause an inappropriate amount of inflammation.

Treg cells are considered to have a protective role against bacterial and fungal infections and also in suppression of autoimmune response. They express forkhead box P3 (FoxP3), CD4, CD25 and produce TGF-β and IL-10. Treg cells do not promote immune function, but act to decrease it instead. Treg cells actively suppress activation of the immune system and prevent pathological self-reactivity. The critical role Treg cells play within the immune system is evidenced by the severe autoimmune syndrome (IPEX syndrome) that results from a genetic deficiency in Treg cells. Despite their low numbers during an infection, Treg cells are believed to play an important role in the self-limitation of the immune system, they have been shown to prevent the development of various autoimmune diseases.