Fig. 9: Treg-depletion causes loss of exocrine function.

a Immunofluorescence labeling of α-amylase and Ki-67 indicates less proliferating acinar cells in the Treg depleted group. Scale bars represent 20 µm. b Quantification of the immunofluorescent labeling confirmed a significantly reduced number of acinar cells (p = 0.0314, PBS n = 6/DT n = 7) and less proliferating Ki67⁺ acinar cells (p = 0.0342, PBS n = 5/DT n = 7) in the pancreas of DT-treated mice. c Gene expression of the pancreatic digestive enzymes amylase (p = 0.0391, PBS n = 9/DT n = 8) and trypsinogen (p = 0.0425, PBS n = 12/DT n = 7) as determined by RT-qPCR was significantly decreased during CP and depletion of Treg cells. Transcript levels as determined by RT-qPCR were normalized using Rn5s as internal calibrator gene and were related to the corresponding mRNA amounts in control mice. d The activity of fecal elastase, a clinical marker of exocrine function, was also significantly decreased in DT-treated mice (p = 0.0280, PBS n = 11/DT n = 10). e The decreased exocrine pancreas function is furthermore reflected in body weight loss. Treg depletion in CP animals significantly increases the weight loss over time (one-way ANOVA p < 0.0001, Bonferroni posttest, con PBS n = 5/DT n = 5, CP PBS n = 7/DT n = 6). All data were presented as means ± SEM, statistically significant differences were tested by unpaired two-tailed students t-test for independent samples and one-way ANOVA, Bonferroni posttest, significance levels of p < 0.05 are marked by an asterisk. Source data are provided as a Source Data file.