Mice lacking the LTB4 receptor BLT1 are protected against autoantibody-induced arthritis.
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...
The Rockefeller University Press
2006
The Rockefeller University Press
2006
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