We demonstrated that activated T cells were increased in LV and lung tissues in HF mice (5), while depletion of CD11c+ antigen-presenting cells or inhibition of the crosstalk between T cells and APCs by CD28 knockout or CD86/CD80 (B7) double knockout significantly attenuated TAC-induced LV hypertrophy and failure (16, 19). This evidence concerns the gene CD86 and cardiac hypertrophy.