Experimental pressure overload induces a cardiac neoantigen specific humoral immune response.

Abstract

Inflammation is a hallmark of heart failure (HF), however anti-inflammatory therapies have yet to translate clinically. T-cells are central to cardiac pathology in experimental models of HF with reduced and preserved ejection fraction (HFrEF and HFpEF), however their antigen requirements differ, as shown in previous studies. Here we demonstrate that pressure overload elicits a cardiac and lymphoid B-cell humoral response characterized by autoantibodies (AAbs) towards the same cardiac neoantigens that induce T-cells in an experimental model of HFrEF, a novel mechanism distinct from an experimental model of HFpEF.