Interleukin-1? (IL-1?) is constitutively produced in osteoarthritis(OA)-affected cartilage and plays a key role in the pathogenesis of the disease by inducing and maintaining an imbalance of cartilage homeostasis and extracellular matrix synthesis. In normal and OA-affected human cartilage, expression of innate antagonist regulators of IL-1 is deficient. Therefore, inhibition of IL-1? action using the IL-1? type II receptor (IL-1RII), which acts as a decoy receptor, would have therapeutic potential. Indeed, IL-1?-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production by chondrocytes, synoviocytes and epithelial cells has been shown to be significantly inhibited by soluble IL-1RII. In this study, the authors have further examined the effects of reconstituting IL-1RII deficient (IL-1RII-) cells with IL-1RII using adenoviral gene transfer.