Mediators of Inflammation / 2015 / Article / Tab 1

Review Article

Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation

Table 1

Qualitative differences in inflammatory cytokine expression in ET, PV, and PMF.

MPN subtypeCytokines produced in excessMain cellular sources

All MPNsIL-6, IL-8, IL-2, soluble IL-2R, HGF, TNF-, TGF-β, GM-CSF, VEGF, and bFGFBone marrow fibroblasts, endothelial cells, monocytes, macrophages, T-lymphocytes, hematopoietic progenitors, and hepatocytes

ETIL-4, IL-10, IFN-γ, MCP-1, PDGF-BB, and soluble IL-6R (gp80)M2 macrophages, platelets, and T-lymphocytes

PVIL-11, IL-12, IL-13, IL-5, and IL-7Bone marrow fibroblasts, T-lymphocytes, M1 macrophages, and hematopoietic progenitors

PMFIL-1β, IL-10, IL-12, IL-13, IL-15, IL-33, G-CSF, IFN-α, MIP-1α, MIP-1β, IP-10, MIG, MCP-1, and PDGF-BBBone marrow fibroblasts, activated T-lymphocytes, neutrophils, macrophages, hematopoietic progenitors, megakaryocytes, and platelets

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