Discovery of a 2-phase Treg specialization process: Naive Tregs in mediastinal lymph nodes differentiate into tissue-resident, reparative Tregs in the heart.
Identification of CCR8 as a definitive marker and functional driver for heart-accumulated Tregs with high immunosuppressive and tissue-repair signatures.
Validation of the CCL1-CCR8 axis: Macrophage-derived CCL1 is essential for the recruitment of CCR8+ Tregs to the infarcted myocardium.
Mechanistic insight into IL-1R2: Tregs facilitate the anti-inflammatory shift of cardiac macrophages by secreting interleukin 1 receptor type 2.
Clinical relevance: Elevated levels of CCR8+ Tregs and CCL1 are confirmed in both circulating blood and cardiac tissues of patients with myocardial infarction.
