There is also an imbalance of T-helper 1 (Th1) and T-helper 17 (Th17) cells compared to T helper 2 (Th2) and regulatory T (Treg cells) (27), and both RA and JIA have been postulated to be mediated by both the type 1 cytokines such as IFN-γ produced and IL-17 (28). This evidence concerns the gene IL17A and rheumatoid arthritis.