Figure 3.

Blockade of DC cross-priming by genetic depletion of Clec9a protects mice from immunopathology after ischemic injury. C57BL/6J (WT) and Clec9a−/−C57BL/6J (KO) mice were treated with 160 mg/kg isoproterenol to induce T2MI-like injury and hearts were isolated for histology and immunohistochemistry. A, cTroponin I levels in serum of WT and KO 24 h after isoproterenol challenge. B, Mononuclear infiltrate/immunopathology and fibrosis in the myocardium of isoproterenol-treated WT and KO mice as assessed by quantification of nuclei in hematoxylin and eosin–stained heart sections over time (day 0, week 2, week 4) after injury. C, Semiquantitative immunopathology score and corresponding changes per mouse strain in myocardial sections of isoproterenol-treated WT and KO mice as assessed by hematoxylin and eosin–stained histology 4 weeks after injury. C, lower, Example micrographs per experimental group. D, Fibrotic area and corresponding changes per mouse strain in myocardial sections of isoproterenol-treated WT and KO mice as assessed by Picrosirius red–stained histology 4 weeks after injury. D, lower, Example micrographs per experimental group. Symbols represent individual mice. Error bars show mean±SEM; *P<0.05; **P<0.001; ***P<0.0001; ****P<0.00001 (2-way ANOVA with Sidak multiple comparisons post hoc test; 2-tailed Student t test for fold-change data [C and D] multiplicity-adjusted P values). Ctrl indicates control; DC, dendritic cell; ISO, isoproterenol; KO, knockout; and WT, wild type.