In the present work, we investigated the mechanism responsible for Lu/BCAM phosphorylation in the presence of JAK2V617F using HEL and BaF3 cell lines as well as RBCs from patients with PV.
CD239 was expressed in a constitutive fashion in PV-derived bone marrow cells and thus a pro-thrombotic function does not seem to be mediated by increased CD239 expression alone.
Our results indicate that JAK2 mutation might be linked to Lu/BCAM modification and increased RBC adhesiveness, which may be a factor favoring thrombosis in PV.