A handshake between platelets and neutrophils might fuel deep vein thrombosis

Deep vein thrombosis (DVT) describes the clogging of veins in extremities, leading to pain, swelling, and potentially life-threatening pulmonary embolism. Although several known factors can provoke DVT, it is not entirely clear how they contribute to thrombus formation. Long-term immobilization of hospitalized patients is thought to provoke DVT through reducing blood flow in the legs. While the associated ischemia activates endothelial cells, two mechanisms drive thrombosis: hypercoagulability caused by the dysregulation of clotting factors, or inflammation caused by the recruitment and activation of immune cells, especially neutrophils. Platelets play an important role in DVT, but how they help to attract neutrophils is incompletely understood. Two independent studies published in the Journal of Thrombosis and Hemostasis and in eLife now provide a fresh perspective on how this might work.