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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier

Fig. 2

Myeloid-specific ikkβ gene deletion alleviates neurological impairment and demyelination in the spinal cord during EAE. a and b The clinical signs for all WT and LysM-Cre/Ikkβ F/F EAE mice were scored (a) and weighed (b) daily for 30 days. c-l Spinal cord sections were obtained from WT (e, i, k, and l) and LysM-Cre/Ikkβ F/F mice (f, j, k, and l) at 15–18 days after immunization, stained with luxol fast blue (c-f) or immunostained with MBP antibody (g-j), and analyzed to measure the degree of demyelination by immunization (k and l). Bars = 10 μm. m and n Spinal cord lysate obtained from WT and LysM-Cre/Ikkβ F/F mice at 15–18 days after immunization were analyzed for the expression of MBP by immunoblotting (m) and were quantified (n). Data are representative of 3 independent experiments with similar results. Data are expressed as mean clinical scores ± SEM. (ANOVA test; *p < 0.05 and **p < 0.01 versus WT EAE mice; #p < 0.05 and ##p < 0.01 versus normal control mice)

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