Figure 7: MiR-125a agomir treatment ameliorates EAE pathogenesis.

(a) Mean clinical scores (±s.e.m.) for EAE induced in 6- to 8-week-old WT mice after three intravenous (i.v.) injections of miR-125a agomir or control agomir (5 μ mol kg⁻¹ per day per mouse) at the onset of EAE. (b) Representative haematoxylin–eosin (H&E) staining or Luxol Fast Blue staining of spinal cord sections on day 21 after immunization of the mice in a. (c) Flow cytometric analysis of the percentage of Treg cells in the CD4⁺ T cells isolated from the CNS of the mice in a on day 21 after immunization. (d) Flow cytometric analysis of the percentages of T_H1 and T_H17 in the CD4⁺ T cells isolated from the CNS of the mice (a) on day 21 after immunization. (e) Mean percentages (±s.e.m.) of Foxp3⁺ Treg cells in the CD4⁺ population of c (n=6 per group). (f) Mean percentages (±s.e.m.) of IL-17⁺ or IFN-γ⁺ T cells in the CD4⁺ population of d (n=6 per group). (g) Mean clinical scores (±s.e.m) for EAE induced in 6- to 8-week-old WT mice with three injections of miR-125a agomir (5 μ mol kg⁻¹ per day per mouse) after acute EAE was established, at a clinical score 1–2. n=7 or 6 per group. The EAE symptoms were evaluated every day. Data are representative of three (a) or two (c–g) independent experiments (mean±s.e.m.). *P<0.05, **P<0.01 (two-tailed Student’s t-test).