Stopping the traffic: a route to arthritis therapy

The trafficking of immune cells to inflamed joints is the hallmark of rheumatoid arthritis. It has been known for years that neutrophils are abundant in the rheumatoid joints and have the potential to inflict tissue damage by the secretion of oxidants and proteases; however, the crucial role of neutrophil trafficking to the joints has only been demonstrated in recent years using transgenic mice and animal models of the disease. This finding opens the door to potential therapies based on inhibition of neutrophil trafficking. In this issue of the European Journal of Immunology, a study reports the use of antisense RNA to knock down the expression of cytosolic phospholipase A2alpha in mice. This has a major effect on neutrophil trafficking into inflamed joints and reverses the inflammatory swelling and tissue damage in the animal model used. This puts cytosolic phospholipase A2alpha, alongside its product leukotriene B4, on the list of potential targets for reducing cell trafficking to the joint in chronic inflammatory diseases like rheumatoid arthritis.