Recent advances in understanding the roles of T cells in pressure overload-induced cardiac hypertrophy and remodeling.

Pressure overload-induced cardiac hypertrophy and remodeling are not simply mechanical responses to overloaded stress. They also involve participation of various immune cells, especially T cells. In this review, we summarized recent advances in understanding the roles of T cells in this process and the possible mechanisms underlying T cells involvement and modulation. In this pathological process, αβT cells play an indispensable role, with contribution of NKT cells and γδT cells. Moreover, among the αβT cells, CD4+ T cells rather than CD8+ T cells are dominant in the process with different subsets exerting diverse influences. Th1 and Th17 cells mainly promote the pathological development, while Treg cells are negative modulators that alleviate cardiac hypertrophy and remodeling. Even though the involvement of T cells has been reported extensively, the detailed modulating mechanism remains to be elucidated. Pressure overload exerting on heart stimulates cytokines secretion from resident cardiac cells and upregulates cell adhesion molecules on cardiac endothelial cells, which together might mediate T cells infiltration into the heart. Infiltrating T cells modulate pro-hypertrophic pathways and the transition from cardiac fibroblasts to myofibroblasts, which might represent mechanisms underlying their effects. Considering the vital participation of T cells, immune regulation is a promising treatment direction for this class of diseases and more work is needed to reveal the detailed mechanism.