title: Not simply misshapen red cells: multimolecular and cellular events in sickle vaso-occlusion.
abstract: 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 JCI, Li et al. explore the regulation of heterotypic neutrophil-platelet contacts in response to TNF-α-induced venular inflammation with relevance to sickle cell disease (SCD).
authors.forename: Gregory M
authors.initials: GM
authors.lastname: Vercellotti
authors.forename: John D
authors.initials: JD
authors.lastname: Belcher
mesh_terms: D000818:Animals; D006801:Humans; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology*; D014657:Vasculitis / Q000503:physiopathology*
chemical_list: C494921:AKT2 protein, human; C494922:Akt2 protein, mouse; D051057:Proto-Oncogene Proteins c-akt