Fig. 7: Crosstalk between immune cells with and without DNMT3A mutations amplifies inflammation contributing to cardiac dysfunction.
From: Cell-intrinsic effects of clonal hematopoiesis in heart failure
Circulating blood cells are recruited to the heart after myocardial infarction. DNMT3A mutant macrophages promote pro-inflammatory activation of wild-type macrophages (macrophage–macrophage axis) and effector differentiation of CD4+ T cells (macrophage–CD4+ T cell axis). DNMT3A mutant NK cells produce elevated levels of pro-inflammatory cytokines and show increased cytotoxic capacity. Both intrinsic activation of immune cells by DNMT3A mutations and indirect activation of wild-type cells by DNMT3A mutant macrophages promote progression of inflammation causing hypertophy and fibrosis, finally resulting in cardiac dysfunction.
