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Figure 1B. Activation or dysfunction of ECs in the myeloproliferative neoplasms (MPNs) changes this milieu to cause activation and adhesion of platelets, leukocytes and red cells to endothelium, formation of circulating plateletleukocyte aggregates, neutrophil extracellular nets (NETs) and microparticles, generation of thrombin, and release of pro-inflammatory cytokines.  The main triggers for this “thromboinflammatory” state are most likely (a) cell-intrinsic abnormalities of platelets, leukocytes, red cells, and ECs as a function of their origin in a mutant hematopoietic clone and (b) the establishment of a pro-inflammatory state, both serving as mutually amplifying factors.