Figure 6.
Figure 6. DCs exacerbate pancreatic fibroinflammation. WT mice were treated with saline, C alone, DCs alone, or C+DCs. (A–C) Paraffin-embedded sections of pancreata were stained with H&E (A) and Picric acid–Sirius red (B), and the fibroinflammatory area per mouse pancreas was calculated for all treatment groups (C). Insets show higher magnification. (D–G) Pancreata were also stained using mAbs directed against amylase (D and E) and insulin (F), and serum glucose (G) levels were calculated. (H–L) Similarly, pancreata were stained using mAbs directed against desmin (H and I), α-SMA (J and K), and CD3 (L). (M) Using flow cytometry, the relative number of intrapancreatic B cells, macrophages, neutrophils, and NK cells in chronic pancreatitis in the context of exogenous DCs expansion was calculated (n = 8–10 mice/group; *, P < 0.05; ***, P < 0.001). Error bars indicate standard error of the mean.

DCs exacerbate pancreatic fibroinflammation. WT mice were treated with saline, C alone, DCs alone, or C+DCs. (A–C) Paraffin-embedded sections of pancreata were stained with H&E (A) and Picric acid–Sirius red (B), and the fibroinflammatory area per mouse pancreas was calculated for all treatment groups (C). Insets show higher magnification. (D–G) Pancreata were also stained using mAbs directed against amylase (D and E) and insulin (F), and serum glucose (G) levels were calculated. (H–L) Similarly, pancreata were stained using mAbs directed against desmin (H and I), α-SMA (J and K), and CD3 (L). (M) Using flow cytometry, the relative number of intrapancreatic B cells, macrophages, neutrophils, and NK cells in chronic pancreatitis in the context of exogenous DCs expansion was calculated (n = 8–10 mice/group; *, P < 0.05; ***, P < 0.001). Error bars indicate standard error of the mean.

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