IL-33 levels were related to the severity and activity of RA.  IL-33 enhanced TNF-α-dependent effects in synovial fibroblasts.  ST2−/− and ST2 neutralization in the CIA model alleviated arthritis symptoms, while administration of IL-33 exacerbated.  IL-33 stimulates mast cells to produce pro-inflammatory factors.  IL-33 stimulated macrophages and synovial cells to produce chemokines, which recruited neutrophils. The gene discussed is TNF; the disease is arthritic joint disease.