Aberrant activation of β1 and β2 integrins on leukocytes in JAK2-V617F mutated disease (A20)

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A20 investigates the activation of integrins on leukocytes in JAK2-V617F-positive chronic myeloproliferative neoplasia (CMN). JAK2-mutated CMN is characterized by clonal proliferation of myeloid cells and a striking inflammatory syndrome. In the previous funding period, we found that JAK2-V617F aberrantly activates β1 and β2 integrins (VLA4 and LFA1) on leukocytes in CMN and identified the molecular mechanisms involved. Using the Vav1-Cre x JAK2+/V617F knock-in mouse model established in our laboratory, we aim to dissect the contribution of aberrant integrin activation for the JAK2-V617F- induced cytokine dysregulation, splenomegaly and pro-thrombotic state.