T cell subsets orchestrate post-myocardial infarction remodeling by modulating inflammation, apoptosis, and fibrosis, highlighting CAR-T and Treg transfer as promising immunotherapeutic strategies.
Abstract: The pathological course of myocardial infarction (MI) entails a complex interplay between innate and adaptive immunity. Although innate immunity plays a dominant role in the tissue damage and clearance during the acute phase, recent studies have shown that T cells also play an important role in myocardial injury and remodeling. Advances in detection technologies have enabled the identification of several autoantigens and clarified the mechanistic roles of distinct T-cell subsets (such as regulatory T cells, helper T cells, cytotoxic T cells, and γδ T cells) during the remodeling phase. These T cell subsets are widely involved in myocardial inflammation, apoptosis and myocardial fibrosis, and play an important role in myocardial remodeling. This review synthesizes current progress on the repertoire of autoantigens recognized after MI, the mechanistic underpinnings of T-cell responses in myocardial remodeling, and emerging immunotherapeutic strategies aimed at mitigating adverse remodeling. Together, these insights provide a conceptual framework to guide future research and therapeutic development in this field. Keywords: myocardial infarction, T lymphocytes, myocardial remodeling, autoantigen, myocardial inflammation
Guo et al. (Sun,) conducted a review in Myocardial Infarction. T cell subsets orchestrate post-myocardial infarction remodeling by modulating inflammation, apoptosis, and fibrosis, highlighting CAR-T and Treg transfer as promising immunotherapeutic strategies.