Fallarino, F., C. Volpi, T. Zelante, C. Vacca, M. Calvitti, M. C. Fioretti, P. Puccetti, L. Romani, and U. Grohmann. 2009. IDO mediates TLR9-driven protection from experimental autoimmune diabetes. J. Immunol. 183: 6303–6312.

In Fig. 1B, the color key was incorrect. The results and conclusions of the article remain unchanged. The corrected Fig. 1B is shown below. The published legend for Fig. 1 is correct, but is shown again for reference.

FIGURE 1.

Higher susceptibility to STZ-induced diabetes in Tlr9−/− mice. WT (n = 12), Tlr3−/− (n = 10), and Tlr9−/− (n = 10) C57BL/6 mice were injected with STZ from day 1, and blood glucose was monitored over time (in A–C, one experiment is depicted of two with similar results). Diabetes was diagnosed in mice with blood glucose level >250 mg/dl. Mice were sacrificed at different times and analyzed for insulinemia (D) and pancreas histology (E and F) and immunohistochemistry (E). A, Average blood glucose in different groups is plotted over time. Data are presented as mean glucose levels ± SD. *, p < 0.01 (Tlr9−/− vs WT mice). B, Blood glucose concentrations over time in individual WT and Tlr9−/− mice. C, Incidence of diabetes over time in TLR-deficient and WT mice. p < 0.01 (Tlr9−/− vs WT mice). D, Blood insulin was measured by ELISA at day 30. Control, control animals treated with vehicle alone. Data are means ± SD of three experiments. *, p < 0.05 (STZ-treated Tlr9−/− vs WT mice). E and F, Pancreatic tissues were processed for H&E staining to evaluate insulitis (E and F) and immunostained for insulin (red, E). In fluorescent images, nuclei were counterstained with 4′,6-diamidino-2-phenylindole (blue). Representative islet area for each group (E) at day 40 and the percentages of islets per mouse with different score (F, see Materials and Methods) of lymphocyte infiltration (days 14 and 40) are shown. Percentages represented number of islets of a given score (see Materials and Methods) over total number of islets (30–40 per pancreas). *, p < 0.01 and **, p < 0.001 (Tlr9−/− vs WT mice).

FIGURE 1.

Higher susceptibility to STZ-induced diabetes in Tlr9−/− mice. WT (n = 12), Tlr3−/− (n = 10), and Tlr9−/− (n = 10) C57BL/6 mice were injected with STZ from day 1, and blood glucose was monitored over time (in A–C, one experiment is depicted of two with similar results). Diabetes was diagnosed in mice with blood glucose level >250 mg/dl. Mice were sacrificed at different times and analyzed for insulinemia (D) and pancreas histology (E and F) and immunohistochemistry (E). A, Average blood glucose in different groups is plotted over time. Data are presented as mean glucose levels ± SD. *, p < 0.01 (Tlr9−/− vs WT mice). B, Blood glucose concentrations over time in individual WT and Tlr9−/− mice. C, Incidence of diabetes over time in TLR-deficient and WT mice. p < 0.01 (Tlr9−/− vs WT mice). D, Blood insulin was measured by ELISA at day 30. Control, control animals treated with vehicle alone. Data are means ± SD of three experiments. *, p < 0.05 (STZ-treated Tlr9−/− vs WT mice). E and F, Pancreatic tissues were processed for H&E staining to evaluate insulitis (E and F) and immunostained for insulin (red, E). In fluorescent images, nuclei were counterstained with 4′,6-diamidino-2-phenylindole (blue). Representative islet area for each group (E) at day 40 and the percentages of islets per mouse with different score (F, see Materials and Methods) of lymphocyte infiltration (days 14 and 40) are shown. Percentages represented number of islets of a given score (see Materials and Methods) over total number of islets (30–40 per pancreas). *, p < 0.01 and **, p < 0.001 (Tlr9−/− vs WT mice).

Close modal