Fig. 3.

Clec9a^creIrf4^fl/fl mice do not show altered susceptibility to cisplatin-induced AKI. (A–F) Kidneys from Clec9a^cre/creIrf4^fl/fl or littermate control mice were analyzed by flow cytometry. Total kidney leukocytes (A) as well as number (B) and frequency (C) of the indicated populations per kidney (SI Appendix, Fig. S2) were calculated and plotted. (D–F) Kidney cDC1, cDC2, CD11b^hi, and F4/80^hi MPs as well as B cells as specificity control were analyzed for GFP and IRF4 expression by flow cytometry. (D) GFP levels and (E) the frequency of GFP-positive cells within each population are shown to indicate excision of the floxed allele. Gray traces represent GFP fluorescence in littermate controls (Clec9a^wt/wtIrf4^fl/fl). (F) IRF4 protein was revealed by intranuclear staining with an anti-IRF4 antibody. Gray traces represent staining with isotype-matched control antibody. (G and H) Cisplatin-induced AKI in Clec9a^wt/wtIrf4^fl/fl and Clec9a^cre/creIrf4^fl/fl mice. (G) Schematic representation of experimental design. Mice were injected with 20 mg/kg b. w. cisplatin and analyzed 72 h later. (H) Serum creatinine and BUN levels are shown. Each dot represents one mouse. Data are representative of two independent experiments with n = 3 and similar results. Horizontal bars represent mean, error bars represent SD, and **P < 0.01.