Abstract Heart failure (HF) is a leading cause of morbidity and mortality. Studies in animal models and individuals with HF revealed a prominent role for CD4+ T cell immune responses in the pathogenesis of HF and highlighted an active cross-talk between cardiac fibroblasts and interferon (IFN)-γ-producing CD4+ T cells that results in profibrotic myofibroblast transformation. Whether cardiac fibroblasts concomitantly modulate pathogenic cardiac CD4+ T cell immune responses is unknown.
