Department of Medicine, Thrombosis and Hemostasis Program, Division of Hematology and Oncology, University of North Carolina, Chapel Hill, North Carolina, USA.
Address correspondence to: Nigel Mackman, Department of Medicine, Thrombosis and Hemostasis Program, Division of Hematology and Oncology, University of North Carolina, 933 Mary Ellen Jones Building, 98 Manning Drive, CB 7035, Chapel Hill, North Carolina 27599, USA. Phone: 919.843.3961; Email: email@example.com.
First published August 13, 2018 - More info
RBCs are the most abundant circulating cells in humans and typically comprise 35% to 45% of the blood volume (hematocrit). Anemia is associated with an increase in bleeding, and epidemiological studies have shown an association between an elevated hematocrit and thrombosis. RBCs may contribute to hemostasis and thrombosis via mechanisms that include platelet margination leading to an increase in the near-wall platelet concentration, blood viscosity, thrombin generation, and platelet activation. In this issue of the JCI, Klatt et al. report that binding of the Fas ligand FasL on the surface of platelets to its cognate receptor FasR on the surface of RBCs increases thrombin generation in vitro and thrombosis in mouse models. This represents a new mechanism by which RBCs contribute to thrombosis.
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