MOG35-55/I-A^b dimer delays onset and reduces severity of EAE <i>in vivo</i>.

<p>Female C57BL/6 wild-type mice were immunized with MOG35-55 to induce paralyzed EAE. PBS, excess MOG35-55 peptide, Mulv env145-158/I-A^b dimer (1 µg per mouse) or MOG35-55/I-A^b dimer (1 µg per mouse) was administered i.p. starting at day 9 post-immunization. Treatments lasted 4 days. (A) Data are expressed as mean clinical scores ± SD (n = 10 for PBS and MOG35-55/I-A^b dimer-treated groups, n = 8 for excess MOG35-55 and Mulv env145-158/I-A^b dimer-treated groups). Black arrows indicate i.p. injection. The mean clinical score in MOG35-55/I-A^b dimer-treated group is lowest (<i>P<</i>0.05), whereas there is no difference among PBS, excess MOG35-55 and Mulv env145-158/I-A^b dimer-treated groups. (B–C) Spinal cord sections obtained from the above four groups at day 25 post-immunization were analyzed for degree of inflammation by H&E and for demyelination by LFB (original magnification 200×). (B) The MOG35-55/I-A^b dimer-treated group showed minimal inflammatory cell infiltration and demyelination. One representative sample from each group is depicted. (C) Semi-quantitative analyses of inflammation and demyelination in spinal cords from four groups were conducted. Histopathological scores were determined as described in <i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047435#s4" target="_blank">Materials and Methods</a></i> and are presented as mean ± SD from 4 mice. Data presented are representative of two independent experiments. Differences between groups were assessed by Mann-Whitney U test. *, <i>P<</i>0.05; **, <i>P<</i>0.01 and n.s., nonsignificant.