Table 1.

Up-regulation of inflammatory cytokines in MPN (inspired by [13,20,24,25]).

		References
Cytokine	Main Function	PV	ET	MF
IL-1β *	Pro-inflammatory, acute phase, stimulating TH/B-cells, proliferation, apoptosis, and differentiation	[26,27]	[26,27]	[21,26,27,28,29,30]
IL-1Ra *	Blocking IL-1	[27,28]	[27]	[21,27,28,31]
IL-5	Growth factor of eosinophils, enhancing B-cell proliferation, and antibody production	[26,27,28,29]	[26,27,28]	[26,27,28,32]
IL-6 *	Pro- and anti-inflammatory, acute phase, differentiation, and cytokine production	[26,27,28,29,33,34]	[26,27,29,33,34]	[21,26,31,33,34]
IL-8 *	Chemotaxis, activating and degranulating neutrophils, and angiogenesis	[27,28,29,33,35]	[27,29,33]	[21,27,31]
IL-10	Anti-inflammatory and inhibition of pro-inflammatory cytokines	[26,27,32,33]	[26,29,33]	[21,26,27,28,29]
TNF-α *	Pro-inflammatory, acute phase, cytokine production, proliferation, and apoptosis	[26,27,29,33,36]	[26,27,29,33,36,37]	[21,26,27,28,30,31,36,37]
IFN-α *	Anti-viral	[26,27]	[26,27]	[21,26,27,28,29]
IFN-γ *	Promoting TH1 and the cellular immune response and activating macrophages	[26,27,28,33]	[27,29,33]	[26,27,30,31]
TGF-β *	Inhibiting growth, activating leucocytes, inducing TReg, apoptotic, antiangiogenic, and healing wounds	[29,38]	[29,38]	[38]
VEGF	Vascular growth factor: vasculogenesis and angiogenesis	[27,28,29,33,39]	[27,29,33,39]	[21,27,28,31,32,39]
CCL2 (*) (MCP-1)	Recruiting monocytes, activating macrophages, histamine release of basophilic cells, stimulating TH2	[28,33]	[27,29,33]	[21,27,29]
CCL3 (MIP1-a)	Stimulating TH1 and DC	[26,28]	[26]	[21,26,28,29,31]
CCL4 (MIP1-b)	Stimulating DC	[26,27,28]	[26,27]	[21,27,29,40]
CXCL9 (MIG)	Activation of the acquired immune system	[27,28,32]	[27,32]	[21,27,28,29,32]
CXCL10	Pro-inflammatory, anti-angiogenetic, and stimulating TH1	[26,27,28,32,36]		[21,26,27,28,29,36]

Summary of the most described up-regulated cytokine levels in the peripheral blood of JAK2-V617F-positive polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF) patients compared to healthy controls. In a recent review, it was mentioned that “a useful correlation of cytokine profiles with driver mutations is currently impossible to generate, since only scattered and not univocal associations have been reported” [20]. This suggests that “somatic mutations in the MPN clone are not the only determinant of the MPN inflammatory state” [20]. * Evidence for involvement in thrombus formation [28,41,42,43].