Mice lacking the LTB4 receptor BLT1 are protected against autoantibody-induced arthritis.

Arthritic joints are chock-full of activated immune cells. These cells produce chemotactic proteins that lure other cells into the joint, setting up a vicious cycle of inflammation. But what instigates this cycle in the first place? A study by Kim et al. (page 829) puts much of the blame on neutrophils.

Neutrophils—granular cells that are among the immune system's earliest responders during infection and injury—are required for the development of joint inflammation during autoantibody-induced arthritis in mice. But the signals that trigger this joint invasion had not been identified.

Kim and colleagues now identify a chemotactic lipid called leukotriene B4 (LTB4) as the instigating signal. In the absence of the receptor for LTB4 (called BLT1), neutrophils failed to invade the joints, and mice did not develop arthritis. This...

You do not currently have access to this content.