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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Beneficial effects of curtailing immune susceptibility in an Alzheimer’s disease model

Fig. 3

Panel a: effects of the treatment with an anti-TNFSF10 monoclonal antibody on the expression of either TNFSF10, TNFRSF10B receptor, proinflammatory, and anti-inflammatory molecules in the spleen of 3xTg-AD mice. Left blots: changes in the expression of TNFSF10 and its TNFRSF10B receptor, as well as in GITR and Foxp3 and the anti-inflammatory cytokine IL-10 expression in 3xTg-AD mice, following chronic treatment (12 months) with an anti-TNFSF10 monoclonal antibody (10 μg/animal twice a month, i.p.) or vehicle (10 μg/animal twice a month, i.p.). Right blots: changes in the expression of the proinflammatory mediators COX2, iNOS, IL-1β, TNF-α in 3xTg-AD mice, following chronic treatment (12 months) with an anti-TNFSF10 monoclonal antibody or vehicle (10 μg/animal twice a month, i.p.). Panel b: densitometric analysis of respective western blots. *p < 0.05 vs untreated 3xTg-AD mice; **p < 0.05 vs. all other matching groups (one-way ANOVA, followed by a Duncan’s multiple range test). Vertical bars are means ± S.E.M. Panel c: representative immunofluorescence photographs of mice spleens for GITR (red) and FoxP3 (green) expression and co-localization of the two molecules (white arrows; merge column; DAPI = nuclear staining) in WT and 3xTg-AD animals receiving either vehicle or an anti-TNFSF10 monoclonal antibody (10 μg/animal twice a month, i.p.) for 12 months. WT wild-type mice (n = 5/group); AD: 3xTg-AD mice (n = 5/group)

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