Fig. 1
EHD2-scTNFR2 enhances the therapeutic effect of ATROSIMAB on EAE. Hu/m TNFR1-ki x hu/m TNFR2-ki mice were immunized with MOG35-55 and treated either with saline (n = 13), EHD2-scTNFR2 (TNFR2 agonist; n = 8), ATROSIMAB (TNFR1 antagonist; n = 11) or a combination (E + A; n = 9). Schematic representation of EAE induction, development and treatment regimen (A). EHD2-scTNFR2 [10 mg/kg] was injected i.p. at 6, 9 and 12 days post-immunization (dpi; blue and green arrows) while ATROSIMAB [20 mg/kg] was injected at 12, 15 and 18 dpi (red and green arrows). Body weight (BW; B) and disease development (C) were measured daily until 25 dpi. EAE development is represented as sum of EAE scores over 25 days (D) but also as mean score at the different treatment days and at killing day (E). On the first day of symptoms, disease onset was recorded (F). Linear regression curves of disease development (C) are shown together with dashed lines representing 95% confidence intervals. Statistical difference between slopes is shown at the bottom right of the graph. Data are presented as mean ± SEM and differences between groups were assessed with Mann–Whitney or Kruskal–Wallis tests, except for relative body weight for which two-way ANOVA and Tukey’s post-test were used. # = PBS vs E + A; $ = PBS vs ATROSIMAB. */#/$p < 0.05, **/##/$$p < 0.01