ArticleThe Journal of clinical investigation2022
CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 45 citations in OpenAlex.
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Myocardial immune vulnerability unmasked after treatment with immune checkpoint inhibitors: a case report.European heart journal. Case reports · 2026Article
- Regulatory T cells sabotage anti-tumor γδ T cells by creating IL-2-deficient environments.The Journal of experimental medicine · 2026Article
- Downexpression of miR- 17 - 5p and miR- 125a- 5p is Potentially Associated with the Renal Impairment Through STAT- 3 and CD69 in Multiple Myeloma Adult Patients.Biochemical genetics · 2026Article
- Constitutively Active Stat5b Expression in Dendritic Cells Enhances Treg-Mediated Elimination of Autoreactive CD8International journal of molecular sciences · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Adaptive immune response to the autoantigen LL-37 differentiates atherosclerotic cardiovascular disease phenotypes.Clinical & translational immunology · 2026Article
- Integrated Transcriptomic, Proteomic, and Network Pharmacology Analyses Unravel Key Therapeutic Mechanisms of Xuebijing Injection for Severe Acute Pancreatitis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Regulatory T cells in homeostasis and disease: molecular mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Finerenone effects on biomarkers: an analysis from the FIGARO-DKD trial.European heart journal · 2025Article
- Immunoregulatory Endothelial Cells Interact With T Cells After Myocardial Infarction.Circulation research · 2025Article
- TRIM13 prevents cardiomyocyte injury by affecting apoptosis through interacting with CD3D in myocardial infarction.iScience · 2025Article
- Regulation of transcription factor function by purinergic signalling in cardiovascular diseases.Purinergic signalling · 2025Review
- AREGMolecular medicine (Cambridge, Mass.) · 2025Article
- A Single-Cell Transcriptome Atlas Characterizes the Immune Landscape of Human Testes During Aging.Aging cell · 2025Article
- CD103+CD56+ ILCs Are Associated with an Altered CD8+ T-cell Profile within the Tumor Microenvironment.Cancer immunology research · 2025Article
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- Comprehensive macro and micro views on immune cells in ischemic heart disease.Cell proliferation · 2024Review
Corrections and comments
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Authors and funding
25 authors at 7 institutions in 2 countries.
Funding
Abstract
Increasing evidence has pointed to the important function of T cells in controlling immune homeostasis and pathogenesis after myocardial infarction (MI), although the underlying molecular mechanisms remain elusive. In this study, a broad analysis of immune markers in 283 patients revealed significant CD69 overexpression on Tregs after MI. Our results in mice showed that CD69 expression on Tregs increased survival after left anterior descending (LAD) coronary artery ligation. Cd69-/- mice developed strong IL-17+ γδT cell responses after ischemia that increased myocardial inflammation and, consequently, worsened cardiac function. CD69+ Tregs, by induction of AhR-dependent CD39 ectonucleotidase activity, induced apoptosis and decreased IL-17A production in γδT cells. Adoptive transfer of CD69+ Tregs into Cd69-/- mice after LAD ligation reduced IL-17+ γδT cell recruitment, thus increasing survival. Consistently, clinical data from 2 independent cohorts of patients indicated that increased CD69 expression in peripheral blood cells after acute MI was associated with a lower risk of rehospitalization for heart failure (HF) after 2.5 years of follow-up. This result remained significant after adjustment for age, sex, and traditional cardiac damage biomarkers. Our data highlight CD69 expression on Tregs as a potential prognostic factor and a therapeutic option to prevent HF after MI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.