The study identifies a forward-feed loop involving macrophage-T cell interactions, IFN-γ, and MCP-1 that drives Ang II-induced cardiac inflammation and fibrosis.
Reciprocal interaction between macrophages and T cells in heart stimulates IFN-γ expression, leading to increased MCP-1 expression in macrophages, which results a forward-feed recruitment of macrophages, thus contributing to Ang II-induced cardiac inflammation and fibrosis.
Han et al. (Wed,) studied this question.