Inflammation contributes to the development of heart failure (HF) through multiple mechanisms including regulating extracellular matrix (ECM) degradation and deposition. Interactions between cells in the myocardium orchestrates the magnitude and duration of inflammatory cell recruitment and ECM remodeling events associated with HF. More recently, studies have shown T-cells have signficant roles in post-MI wound healing. T-cell biology in HF illustrates the complexity of cross-talk between inflammatory cell types and resident fibroblasts. This review will focus on T-cell recruitment to the myocardium and T-cell specific factors that might influence cardiac wound healing and fibrosis in the heart with consideration of age and sex as important factors in T-cell activity.

炎症通过多种机制促进心力衰竭（HF）的发展，包括调节细胞外基质（ECM）降解和沉积。心肌细胞之间的相互作用协调了与心力衰竭相关的炎症细胞募集和 ECM 重塑事件的程度和持续时间。最近，研究表明 T 细胞在心肌梗死后伤口愈合中发挥着重要作用。心衰中的 T 细胞生物学说明了炎症细胞类型和常驻成纤维细胞之间串扰的复杂性。本综述将重点关注心肌中 T 细胞的募集以及可能影响心脏伤口愈合和心脏纤维化的 T 细胞特定因素，同时考虑年龄和性别作为 T 细胞活性的重要因素。