Thrombosis is a major problem for patients with myeloproliferative neoplasms (MPNs). Leukocytes have long been speculated to contribute to thrombotic development in MPNs, but the exact role of these cells has not been fully elucidated. In this issue of the JCI, Edelmann and colleagues demonstrate that granulocytes from mice expressing an MPN-associated JAK2 mutation (JAK2-V617F) exhibit enhanced adhesion to VCAM1- and ICAM1-coated surfaces. The increased adhesion was shown to be mediated by β1 (VLA-4) and β2 integrins, which are activated via inside-out signaling induced by JAK2-V617F. In a murine thrombosis model, administration of neutralizing antibodies targeting VLA-4 and β2 integrin reduced thrombosis, suggesting the intriguing possibility that targeting these pathways could have clinical relevance for MPN.

Original languageEnglish
Pages (from-to)4248-4250
Number of pages3
JournalJournal of Clinical Investigation
Issue number10
StatePublished - Oct 1 2018


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