IL-17A signaling through cardiac fibroblasts inhibits Ly6Clo monocyte-to-macrophage differentiation and increases MerTK shedding on Ly6Chi monocyte-derived macrophages, promoting a pro-inflammatory state in myocarditis.
Cardiac fibroblasts play a decisive role in monocyte-derived macrophage ontogeny and function during cardiac injury, with IL-17A signaling inhibiting Ly6Clo differentiation and promoting pro-inflammatory Ly6Chi macrophages.
MDMs are associated with the reduction of cardiac fibrosis and prevention of the myocarditis sequalae.
Hou et al. (Mon,) conducted a other in Myocarditis. IL-17A signaling vs. IL-17A deficiency or absence of signaling was evaluated on Monocyte-to-macrophage differentiation and MerTK expression. IL-17A signaling through cardiac fibroblasts inhibits Ly6Clo monocyte-to-macrophage differentiation and increases MerTK shedding on Ly6Chi monocyte-derived macrophages, promoting a pro-inflammatory state in myocarditis.