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Mice lacking the LTB4 receptor BLT1 are protected against autoantibody-induced arthritis.
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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 effect was reversed when wild-type neutrophils were transferred into the deficient mice. Consistent with these data, a study by Chen et al. (page 837) shows that LTB4 is essential for disease induction in the same model.
Once in the joint, the neutrophils triggered the production of chemokines that attracted other cells—including more neutrophils—to the area. BLT1 expression was mandatory only for the initial vanguard of neutrophils that infiltrated the joint; it was dispensable for those that followed—presumably because other neutrophil-attracting chemokines were produced.
According to Chen et al., neutrophils were also the primary producers of LTB4. But what entices the first neutrophils to enter the joint and, once there, what signals cause them to produce LTB4 are still unknown. 
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