In human fibroblast-like synoviocytes from RA patients, VIP downregulated the expression and production of proinflammatory cytokines, chemokines and COX2 as well as the production of IFNβ, CXCL8, and the matrix metalloproteinase-3 induced by TLR ligands [16], [17], [28]. This evidence concerns the gene CXCL8 and rheumatoid arthritis.