DC functional impairment drives myeloproliferative disease. WT and CD11c^ΔMHCII mice were assessed by flow cytometry at 12 weeks, 20 weeks, 30 weeks, and 1 year of age. (A) Representative line graph of MHCII in splenic CD11c⁺ cells in wild-type and CD11c^ΔMHCII mice. (B) Percentage of cDCs in WT and CD11c^ΔMHCII mice at 12 weeks (n = 11, 13), 20 weeks (n = 22, 16), 30 weeks (n = 18, 14), and 1 year (n = 22, 25) of age. (C) Plasmacytoid DCs in WT and CD11c^ΔMHCII mice at 12 weeks (n = 6, 11), 20 weeks (n = 15, 12), 30 weeks (n = 3, 3), and 1 year (n = 16, 19) of age. (D) WT and CD11c^ΔMHCII mice were assessed for body weight at 12 weeks (n = 11, 13), 20 weeks (n = 21, 16), 30 weeks (n = 19, 13), and 1 year (n = 24, 25) of age and (E) for spleen weight at 12 weeks (n = 11, 13), 20 weeks (n = 22, 16), 30 weeks (n = 20, 16), and 1 year (n = 23, 25) of age. Dashed line indicates threshold for splenomegaly (2 standard deviations above the mean of WT mice from all age groups). Median and individual data points are shown. (F) Cumulative incidence plot of splenomegaly over time in WT and CD11c^ΔMHCII mice using a Kaplan-Meier curve (all mice were censored at the time of analysis). The log-rank test was used for comparison between curves.