Cytokines are essential in regulating the immune system and inflammatory responses. In the pathogenesis of MPNs, they play a crucial role in advanced stages of the disease, such as myelofibrosis. In this study, Dunbar et al identify the CXCL8/CXCR2 cytokine signaling axis as a key mediator of bone marrow fibrosis in MPNs, suggesting potential therapeutic strategies.
Cytokines are key proinflammatory messenger molecules that help to regulate the immune system and inflammatory responses. They are well established in the pathogenesis of myeloproliferative neoplasms (MPNs), including in advanced stages of disease, such as myelofibrosis (MF).(1) In this issue of Blood, Dunbar et al identify the chemokine (C-X-C motif) ligand 8 (CXCL8)/CXCR2 cytokine signaling axis as a key mediator of bone marrow fibrosis in MPNs, providing a therapeutically tractable avenue to prevent or treat this lethal complication of MPNs.(2)
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