Thromboinflammatory diseases result from the interactions of vascular endothelial cells, inflammatory cells, and platelets with cellular adhesion molecules, plasma proteins, and lipids. Tipping the balance toward a prothrombotic, proinflammatory phenotype results from multicellular activation signals. In this issue of the
Gregory M. Vercellotti, John D. Belcher
Conceptual model of molecular and cellular interactions that influence the development of vaso-occlusion in SCD mice.