MPN disease parameters upon 3 weeks of treatment using an αTNFR2 antibody. JAK2^+/VF mice were treated intraperitoneally, 5.0 mg/kg body weight, 2 times a week for 3 weeks with an anti-mouse TNFR2 antibody (clone TR75-54.7) or polyclonal Armenian Hamster IgG as control antibody. Blood counts were analyzed weekly during the treatment phase. All mice were 12 to 13 weeks old at the end of therapy JAK2^WT and JAK2^+/VF mice were age matched (11-15 weeks). (A-F) HCT and blood count analysis of untreated JAK2^+/VF mice (n = 15), JAK2^WT mice (n = 14), and JAK2^+/VF mice treated with αTNFR2 antibody (n = 5) or IgG (n = 4). (B) Change in HCT (ΔHCT) in αTNFR2-treated mice and corresponding control group. Differences between HCT at the start and end of treatment in αTNFR2-treated mice and IgG-treated controls (ΔHCT = HCT_End − HCT_Start). (G) Spleen weights for untreated JAK2^+/VF mice (n = 11), JAK2^WT mice (n = 10), and JAK2^+/VF mice treated with αTNFR2 antibody (n = 5) or IgG (n = 4). (H) Representative photographs of spleens from untreated control mice (n = 3) and JAK2^+/VF mice (n = 6) treated with αTNFR2 antibody (n = 2) or IgG (n = 2). *P < .05, **P < .01, ***P < .001 ****P < .0001. Ctrl, control; ns, not significant.