IL-11Rα^−/− mice are more resistant to the protective effects of IVIg treatment during EAE.

<p>EAE was induced in C57BL/6J IL-11Rα^+/+ littermates (WT) or IL-11Rα^−/− mice that were administered IVIg or HSA (1 g/kg) daily beginning on the day of EAE induction. Mice were followed for clinical signs and a histological analysis of inflammation and demyelination was conducted at the end-point of the experiment. <b><i>A</i></b>, shows the mean + SEM clinical scores of mice over a time-course of EAE. The graph shows combined data from three consecutive EAE studies that each contained (N = 5–10 mice/group). <b><i>B</i></b>, shows representative spinal cord sections from control- or IVIg-treated IL-11Rα^−/− or WT mice stained with haematoxylin and eosin and luxol fast blue. <b><i>C</i></b>, shows the percent quadrants of spinal cords (N = 10 sections/mouse) that were positive for meningitis or perivascular cuffs in EAE mice. <b><i>D</i></b>, shows the percent demyelination in these spinal cord sections. Values in <b><i>C & D</i></b> are means + SEM of N = 4–6 mice per group for one representative experiment. *represents a significant difference (*p<0.05) from the HSA-treated, genotype-matched counterpart as determined by one-way ANOVA and a Tukey post-hoc test.