T Cell Responses in Ischemic Heart Disease and Cardiac Inflammation

Ischemic heart disease is a common consequence of coronary artery disease (CAD), which is primarily driven by atherosclerosis, a chronic inflammatory condition characterized by lipid accumulation and immune cell infiltration in arterial walls. T cells play a central role in CAD progression and post-ischemic cardiac remodeling, influencing both myocardial healing and tissue damage. Inflammation-driven T cell activation contributes to plaque formation and destabilization, while regulatory T cells (Tregs) help maintain immune balance. However, in the atherosclerotic microenvironment, Tregs can convert into pro-inflammatory exTregs, potentially exacerbating disease progression.

Beyond atherosclerosis, T cells are also key players in cardiac inflammation, including myocarditis, where excessive T cell activation can drive myocardial injury and heart failure. Cytotoxic T cells contribute to viral clearance but can also mediate cardiac damage, while an imbalance between Th17 cells and Tregs influences disease severity. Understanding immunological dynamics of T cells and their crosstalk with other immune components like dendritic cells, is critical for developing targeted therapies aimed at modulating T cell responses in CAD and cardiac inflammation.



This research topic aims to explore the multifaceted roles of T cell responses in coronary artery disease and ischemic heart disease, focusing on their contributions to both disease progression and myocardial recovery. We seek to address critical questions such as: What are the disease-relevant antigens and epitopes? How do T cells contribute to myocardial healing versus adverse remodeling? What are the mechanisms driving T cell activation in the context of CAD? What mechanisms drive the plasticity of T cells, allowing Tregs to adopt pro-inflammatory phenotypes? Recent advances in immunotherapy, including the modulation of T cell activity, present exciting opportunities to enhance cardiac repair and improve clinical outcomes. By integrating findings from experimental and clinical studies, this research topic aims to advance our understanding of T cell-mediated mechanisms in CAD and their therapeutic potential.



We invite contributions that delve into various aspects of T cell responses in coronary artery disease, including but not limited to:

• MHC-I and MHC-II restricted disease-relevant epitopes

• Mechanisms of T cell activation, differentiation, and plasticity in CAD

• The role of different T cell subsets (CD4+, CD8+) in atherosclerosis and myocardial injury

• Interactions between T cells and other immune cells in the ischemic and inflamed cardiac microenvironment

• Treg function and the mechanisms underlying their conversion to exTregs in atherosclerosis

• Clinical implications of T cell responses for patient outcomes following ischemic events

• Novel therapeutic strategies in targeting T cell pathways for therapeutic purposes



In this topic, we welcome original research articles, reviews, mini reviews, perspective articles or case studies that contribute to a comprehensive understanding of T cell biology in ischemic heart disease.