Fig. 4: Ruxolitinib treatment decreases inflammatory cytokine levels in sera of ruxolitinib sensitive and resistant JAK2-V617F transplanted mice. | Nature Communications

Fig. 4: Ruxolitinib treatment decreases inflammatory cytokine levels in sera of ruxolitinib sensitive and resistant JAK2-V617F transplanted mice.

From: Efficacy of JAK1/2 inhibition in murine myeloproliferative neoplasms is not mediated by targeting oncogenic signaling

Fig. 4

Serum levels of tumor necrosis factor alpha (TNF-α) (A), interleukin-6 (IL-6) (B), monocyte chemoattractant protein 1 (MCP-1)/chemokine (C-C motif) ligand 2 (CCL2) (C), interferon-beta (IFN-β) (D), and interleukin-27 (E) determined in ruxolitinib vs. vehicle treated JAK2-V617F and JAK2-V617F + L902Q mice (n = 5). Data represent mean ± SEM. P value was calculated using two-tailed Student’s t test. F–J CD11b+ granulocytes of EGFP+ cells from bone marrow of JAK2-V617F and JAK2-V617F + L902Q mice were isolated from vehicle and ruxolitinib treated groups. Microarray analysis was performed on these cells for cytokine landscape. Inflammatory cytokines such as of tumor necrosis factor alpha (TNF-α) (F), IL-6 (G), MCP-1/CCL2 (H), IFN-β (I), and IL-27 (J) were depicted from bone marrow (BM) compartment of the ruxolitinib (n = 4) vs. vehicle (n = 3) treated JAK2-V617F and JAK2-V617F + L902Q mice. Data represent mean ± SEM. Adjusted p value based on Benjamini-Hochberg Step-Up FDR-controlling Procedure. Source data is provided in the Source Data file.

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