These observations illustrate an important feed-forward interaction between Th17 cells and FLSs in the initiation and augmentation of joint inflammation: once arthritogenic Th17 cells are activated and recruited into the joints to initiate inflammation, FLSs further increase CCL20 in response to IL-17 and other pro-inflammatory cytokines, and accelerate the recruitment of Th17 cells to initiate and augment arthritis (24). This evidence concerns the gene IL17A and arthritic joint disease.