Mediators of Inflammation / 2015 / Article / Fig 5

Review Article

Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation

Figure 5

Chronic inflammation in myeloid neoplasms and new therapeutic options. In MPN patients, chronic inflammation includes the participation of JAK2-V617F-, MPL-W515 L/K-, or CALR-mutated cells and the production of inflammation cytokines under the control of these mutations. Chronic inflammation may also be reactive to the MPN clone or to other coexisting causes of inflammation (hypoxia due to cell accumulation in the bone marrow; thrombosis; infection; others). Healthy and mutated (clonal) myeloid cells participate in MPN-associated reactive inflammation, and the NF-κB, JAK/STAT, and HIF pathways are chronically activated in the MPN clone and in cells from the bone marrow environment. Ideally treatment should combine the following: (1) inhibition of the JAK2-V617F, MPL-W515L/K, or CALR mutations, possible with JAK inhibitors; (2) inhibition of chronic inflammation, via the neutralization or inhibition of inflammation cytokines or receptors, and/or the inhibition of the NF-κB and HIF pathways; (3) in cases where chronic inflammation precedes mutation, and a cause is identified, adequate treatment of the initial cause of inflammation could be added (e.g., antibiotics or antiviral treatment in case of latent infection).

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