Fig. 1From: Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer’s diseaseTreg treatment suppress Amyloid pathology. A ELISA quantification of mice brain homogenates shows a trend toward an increased levels of SDS-soluble and formic acid treated insoluble Aβ40 and Aβ42 in 5xFAD-Rag2KO, compared to 5xFAD-WT. Ex vivo expanded Treg administration decreased both soluble and insoluble Aβ40 and Aβ42 burden in 5xFAD-Rag2KO (10-month-old mice, 10 per group; sex-balanced). B, C Representative images of Aβ immunostaining (6E10) of the dentate gyrus (DG) and frontal cortex (FC) in 5xFAD-WT, 5xFAD-Rag2KO and Treg-treated 5xFAD-Rag2KO. D–I Quantification of the 6E10-positive amyloid aggregates in the DG and FC. The percentage of area covered by Aβ in the DG were increased in 5xFAD-Rag2KO compared to 5xFAD-WT. Number of plaques and their signal intensity were comparable between 5xFAD-Rag2KO and 5xFAD-WT in both DG and FC. Ex vivo expanded Treg administration reduced area covered by plaque, number of plaques and their signal intensity in both DG and FC of 5xFAD-Rag2KO mice (n = 6–7 per group). J Immunostaining of Tregs (CD3 in red, Foxp3 in green) and cell nuclei (DAPI in blue) in the DG of 10-month-old 5xFAD-Rag2KO mice treated with human Tregs or Phosphate-buffered saline (PBS). K, L Quantification of number of CD3+Foxp3+ Tregs in the DG and FC of 4 groups of mice including Treg treated 5xFAD-Rag2KO, Treg treated WT-Rag2KO, PBS treated 5xFAD-Rag2KO and also PBS treated WT-Rag2KO mice. Numbers shown as averages ± SEM with one-way ANOVA. P-values are *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Scale bar, 100 μmBack to article page