Fig. 7

Inflammation in the intestinal mucosa of Foxp1^f/fFoxp3^IRES-YFP-Cre mice. a Representative flow cytometric analysis from LI-LP (top) and quantification (bottom) of Foxp3⁺Nrp1⁻Helios⁻ iTreg population within GALT tissues from WT and KO mice. b Representative flow cytometric analysis from LI-LP (top) and quantification of percentage of IL17-producing CD4⁺Foxp3⁻ cells in 6–9-week- (middle panel) and 36–40-week-old (lower panel) WT and KO mice. c Representative histological sections (left) and histological scoring (right) of colon from aged WT and KO mice. Sections were stained with hematoxylin and eosin. Original magnification ×100, scale bar equals 100 µm. d Susceptibility of WT and KO mice to 2% DSS-induced chronic model of colitis. Body weight loss over time is presented as a read out of disease severity. Two-way ANOVA with Bonferroni post-test was applied and statistically significant differences in mean values is considered at P < 0.05. Data are representative of two experiments (n = 10 for each group). e Histological sections (left) and scoring (right) of colon from representative DSS-treated WT and KO mice. Sections were stained with hematoxylin and eosin. Original magnification ×100, scale bar equals 100 µm. f Intracellular staining and quantification of colonic IFN-γ- and IL17-producing CD4⁺Foxp3⁻ cells from representative DSS-treated mice. PP Peyer’s patches, SI small intestine, LI large intestine, mLN mesenteric lymph nodes. Data are representative of 2–4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P<0.0001 (Student’s t test, error bars, s.d.)