Cardiac fibroblasts actively participate in the immunopathogenesis of myocarditis through soluble signals and direct crosstalk with dendritic cells, macrophages, and CD4+ T cells.
The myocardium responds to aetiologically different pathological injuries through a common multistep process involving highly co-ordinated interactions between cardiac and immune cells. Cardiac fibroblast cells which constitute the prevalent cell type in the heart to have their functional effects that express contractile proteins and exhibit increased migratory, proliferative and secretory properties. During the pathogenesis of myocarditis, cardiac fibroblast, dendritic cells, macrophages, CD4(+) T cells and other immune cells are known to play variable roles. It is becoming increasingly clear that cardiac fibroblasts are not passive players in immune responses, and several evidences show this through the release of soluble signals and/or direct interactions with these immune cells. Typically, fibroblasts are involved in synthesizing factors such as cytokines, chemokines, prostanoids, matrix components and matrix-degrading enzymes to influence dendritic cells, CD4(+) T cells and macrophage functions and vice versa in the pathogenesis of myocarditis. Again, evidence proves a crosstalk between cardiac fibroblasts and immune cells recruited into the myocardium during myocarditis in the microenvironments. This piece reviews the properties and roles of cardiac fibroblast cells, dendritic cells, macrophages and CD4(+) T cells in the pathogenesis of myocarditis, and how these cells interplay on each other in the microenvironment.
Amoah et al. (Wed,) conducted a review in Myocarditis. Cardiac fibroblasts actively participate in the immunopathogenesis of myocarditis through soluble signals and direct crosstalk with dendritic cells, macrophages, and CD4+ T cells.