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. Author manuscript; available in PMC: 2016 Mar 3.
Published in final edited form as: Sci Signal. 2015 Mar 3;8(366):ra24. doi: 10.1126/scisignal.aaa2147

Fig 2. Loss of p38α in CNS-resident cells delays EAE progression and impairs the infiltration of inflammatory cells into the CNS.

Fig 2

(A) EAE disease course of MOG-immunized WT and p38αNesCre mice. Data are means ± SEM of 8 to 11 mice per group. (B to D) WT and p38αNesCre EAE mice were analyzed on day 16 after immunization. (B) H&E staining of the indicated regions of the spinal cord. (C) Histology scores of the indicated regions of the spinal cord. (D) Staining of thoracic spinal cords with anti-CD3 antibody (α-CD3), α-Iba1, and Luxol fast blue. Images are 10× original magnification. Data are from five mice per group. (E) Flow cytometric analysis of cells from the spinal cords of WT and p38αNesCre EAE mice on day 16 after immunization. Data are representative of 10 mice per group. (F) Analysis of the relative numbers and percentages of the indicated cell types in the spinal cords of the mice analyzed in (E). *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.