Similarly, antagonizing IL-33's biological effects, using anti-ST2 blocking antibodies, was effective in ameliorating joint inflammation in a murine model of rheumatoid arthritis [46]; in fact, the administration of IL-33 to cultures of immune cells isolated from murine inflamed joints led to a dramatic increase in IL-5, IL-6, and IL-17 production [45, 46]. This evidence concerns the gene IL33 and rheumatoid arthritis.