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. 2012 Aug 27;209(9):1671–1687. doi: 10.1084/jem.20111706

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© 2012 Ochi et al.

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Figure 9. — Fibroinflammatory and dysplastic effects of DCs are exaggerated upon MyD88 inhibition and are contingent on CD4⁺ T cells. (A–C) MyD88^−/− or WT DCs were adoptively transferred to WT mice undergoing caerulein-induced chronic pancreatitis. The extent of fibrosis and acinar destruction (A), as well as PanIN formation (B) and size of the CD4⁺ T cell infiltrate (C) in pancreata of treated animals were determined. Experiments were performed using a mean of five mice per group (**, P < 0.01; ***, P < 0.001). (D and E) Mice deficient in CD4⁺ T cells, CD8⁺ T cells, B cells, Gr1⁺ inflammatory monocytes and neutrophils, or TNF production were induced to develop chronic pancreatitis in the context of DC overexpansion. Pancreatic effacement and fibroinflammatory changes were quantified for each group by examining 10 HPFs per slide (n = 4–6 mice/experimental group; ***, P < 0.001). (F) 4-wk-old p48Cre;Kras^G12D mice were adoptively transferred with DCs or administered saline for 5 wk. Selected cohorts were additionally treated with GK1.5 to deplete CD4⁺ T cells. Pancreas weights were measured (n = 4 mice/experimental group; ***, P < 0.001). Error bars indicate standard error of the mean.