Fig. 1
From: Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis
TNFR modulation ameliorates EAE, reducing demyelination, oligodendrocyte loss and cellular infiltration. hu/m TNFR1ki mice were treated with either PBS (control) (n = 20), 20 mg/kg H398 (n = 24), 10 mg/kg EHD2-sc-mTNFR2 (n = 13) or H398 and EHD2-SC-mTNFR2 (n = 24) on days 1, 4, 8, 12 and 16 of manifest EAE and followed until day 20 of EAE (A). Cumulative EAE scores (B) and evaluation of EAE-associated weight loss (C) were then assessed. hu/m TNFR1ki mice treated with either PBS (D, I, N, S; n = 10), H398 (E, J, O, T; n = 10), EHD2-sc-mTNFR2 (F, K, P, U; n = 8) or H398 and EHD2-SC-mTNFR2 (G, L, Q, V; n = 9) were killed at day 20 of EAE. Spinal cord sections were assessed for either H demyelination using LFB, M the density of CC1-positive oligodendrocytes, R CD3-positive T cell infiltration, or W the density of Mac-3-positive macrophages/activated microglia. *p < 0.05, **p < 0.01, cumulative score and LFB one-way ANOVA followed by Dunn’s multiple comparison test, CC1, CD3 and Mac-3 one-way ANOVA followed by Dunnett’s multiple comparison test. Scale bars = 100 µm