Fig. 5
Deletion of IGF1R from CNS-resident myeloid cells leads to worsened clinical signs and tissue inflammation in EAE. EAE was induced in tamoxifen-treated IGF-1RWT−tdTomato (n = 13) and IGF-1RKO−tdTomato mice (n = 21) Shown are: A clinical score of disease (mean ± SEM of animals pooled together from 5 independent experiments), statistical analysis: two-way ANOVA, multiple comparisons test of score differences per EAE day between IGF-1RWT−tdTomato and IGF-1RKO−tdTomato mice. B area under the curve (AUC) (Mann Whitney U test, p = 0.001) and C) disease incidence in the immunized mice (Mann Whitney U test, p = 0.999). Data is represented as mean ± SEM. D At the symptomatic peak of disease, CNS tissue was isolated from IGF-1RWT−tdTomato (n = 4) and IGF-1RKO−tdTomato mice (n = 5) and DAPI staining was performed to assess lesion density (number of inflammatory lesions/cm2, unpaired t test with Welch`s correction, p = 0.0335) and Area of individual lesions (μm2). Per mouse, four to five regions have been analysed and the mean was calculated. Each dot represents mean values obtained per mouse. Data is represented as mean ± SEM. (E) Representative image displaying spinal cord lesions in 1RWT−tdTomato and IGF-1RKO−tdTomato mice at peak, white dotted lines indicate single lesions, scale bar 100 μm. (F) Following immunostaining against MBP, the degree of demyelination was quantified, displayed is MBP relative staining intensity. Data is represented as mean ± SEM, ). Representative images displaying MBP + staining of spinal cords at EAE peak in IGF-1RWT−tdTomato and IGF-1RKO−tdTomato, scale bar 100 μm. H Similarly, after immunostaining against the astrocyte marker GFAP, we quantified the degree of astrogliosis (displayed as GFAP + cell density—cells/mm2) I Representative pictures of GFAP + staining in spinal cords at EAE peak in IGF-1RWT−tdTomato and IGF-1RKO−tdTomato, scale bar 100 μm. Asterisks indicate significant differences (∗ p < 0.05, ∗  ∗ p < 0.01 and ∗  ∗  ∗ p < 0.001, ∗  ∗  ∗  ∗ p < 0.0001)