Previous studies have indicated that a number of inflammatory diseases, including rheumatoid arthritis (RA) and IBD, are correlated with an imbalance in Th17 cell/Treg-related cytokines.69,70 An excessive Th17 cell response to pathogens induces increased proinflammatory cytokine IL-17 expression, which in turn stimulates other cells, such as epithelial cells, to produce IL-6, TNF-α, and IL-1, ultimately perpetuating inflammation.54 However, Th17 cell-induced inflammation can be counterbalanced by Tregs. Here, IL1B is linked to rheumatoid arthritis.