CD4 ⁺ T Cells Promote the Transition From Hypertrophy to Heart Failure During Chronic Pressure Overload

Abstract

+ T-cell subsets (CD8KO). In contrast to CD8KO mice, MHCIIKO mice did not develop ventricular dilation and dysfunction. MHCIIKO mice also displayed very low fibrosis, collagen accumulation, and cross-linking within cardiac tissue. Interestingly, mice with transgenic CD4 + T-cell receptor specific for ovalbumin failed to develop HF and adverse remodeling.

Endothelial mineralocorticoid receptor contributes to systolic dysfunction induced by pressure overload without modulating cardiac hypertrophy or inflammation

“…2016) and that T cells are necessary for cardiac inflammation, hypertrophy, and fibrosis in HF induced by TAC, as T‐cell‐deficient mice are protected from these cardiac responses to pressure overload (Laroumanie et al. 2014; Nevers et al. 2015).…”

Cardiac Nonmyocytes in the Hub of Cardiac Hypertrophy

“…It has been recently reported that both CD4 + and CD8 + T cells were increased in number in ventricular myocardium and in mediastinal heart draining lymph nodes in pressure-overloaded mice. 102 In recombination activating gene 2 knockout mice, lack of both T and B cells prevented contractile dysfunction, but not cardiac hypertrophy, after TAC operation. The lack of CD4 + T cells in MHC-II knockout mice also prevented pressure overload−induced cardiac remodeling and failure, but the lack of CD8 + T cells did not.…”

The extracellular matrix in myocardial injury, repair, and remodeling

“…Mechanical stretch has been suggested as triggering purinergic signaling in cardiomyocytes, leading to release of fibrogenic growth factors (107). Moreover, T lymphocytes and macrophages have been implicated in activation of resident cardiac fibroblasts following pressure overload (108,109).…”