Fig. 6.

Subventricular zone-derived Chi3l3 affects EAE severity and oligodendrogenesis. a Protocol of shRNA lentiviral particle (LVP) administration, BrdU injection, and EAE induction. b Clinical score (left) and linear regression curves (right) of mice treated with control shRNA LVPs (black line) or Chi3l3 shRNA LVPs (red line) and immunized with PLP_139–151. Dashed lines indicate 95% confidence intervals. (n = 23 control shRNA LVP and 27 Chi3l3 shRNA LVP mice per group; two-way ANOVA; c Quantifications of percentage (left) and number (right) of NG2⁺/BrdU⁺ double-positive cells in the ipsilateral (IL) and contralateral (CL) SVZ of Chi3l3 shLVP and control shLVP mice killed at onset of disease in vivo. (n = 4 per group; two-tailed Student’s t test; d Quantifications of and number of NG2⁺ cells in the ipsilateral (IL) and contralateral (CL) SVZ of Chi3l3 shLVP and control shLVP mice sacrificed during chronic EAE (n = 8 control shRNA mice, n = 6 Chi3l3 shRNA mice; two-tailed Student’s t test. e, f Localization (left) and quantification of inflammatory lesions in brain sections (middle) and spinal cord sections (right) of Chi3l3 shLVP and control shLVP mice killed at EAE onset (e; n = 4 mice control shRNA, n = 5 mice Chi3l3 shRNA (left, brain), n = 5 mice per group (right, spinal cord; two-tailed Student’s t-test; mean ± s.e.m) and during chronic EAE (f, n = 7 mice control shRNA mice, n = 8 Chi3l3 shRNA mice (left, brain) and n = 8 mice control shRNA mice, n = 6 Chi3l3 shRNA mice (right, spinal cord); two-tailed Student’s t test). Schematic diagram showing localization of inflammatory lesions of individual mice, each color represents an individual mouse. (mean ± s.e.m.; *p < 0.05; **p < 0.01; ***p < 0.005)