Diphtheria toxin (DT)-induced depletion of CD11c+ DCs in irradiated WT recipient mice that received bone marrow transfer from CD11c-DTR/GFP transgenic donor mice significantly blocked TAC-induced cardiac dysfunction along with reduced cardiomyocyte hypertrophy, cardiac fibrosis, LV remodeling, and LV myocardium CD45+ cells, CD11b+ cells, CD8+ T cells, or activated effector CD44+CD8+ T cells at 24 weeks after TAC injury. The gene discussed is ITGAX; the disease is persistent truncus arteriosus.