[HTML][HTML] Not simply misshapen red cells: multimolecular and cellular events in sickle vaso-occlusion

GM Vercellotti, JD Belcher - The Journal of clinical …, 2014 - Am Soc Clin Investig
The Journal of clinical investigation, 2014Am Soc Clin Investig
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).
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).
The Journal of Clinical Investigation