ArticleJournal of the American College of Cardiology2021
Innate Lymphoid Cells Promote Recovery of Ventricular Function After Myocardial Infarction.
Article in Journal of the American College of Cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 47 citations in OpenAlex.
- Anti-inflammatory therapy with low-dose IL-2 in acute coronary syndromes: a randomized phase 2 trial.Nature medicine · 2026Trial
- The impact of pericardial disruption on heart function and remodeling after myocardial infarction in mice.The international journal of cardiovascular imaging · 2026Article
- Review
- Cytokine-mediated, organ-specific immune modulation and dysregulation of innate lymphocytes in sepsis.Seminars in immunopathology · 2026Review
- ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair.Cell communication and signaling : CCS · 2026Article
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Current anti-inflammatory strategies for treatment of heart failure: From innate to adaptive immunity.Pharmacological research · 2025Review
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Differential roles of eosinophils in cardiovascular disease.Nature reviews. Cardiology · 2025Review
- Anti-inflammatory Therapies for Ischemic Heart Disease.Current cardiology reports · 2025Review
- Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Group 2 innate lymphocytes protect the balance between autophagy and apoptosis in cardiomyocytes during sepsis-induced cardiac injury.Scientific reports · 2024Article
- Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation.Cardiovascular research · 2024Article
- Inflammation in acute myocardial infarction: the good, the bad and the ugly.European heart journal · 2024Article
- Type 2 innate lymphoid cells are protective against hepatic ischaemia/reperfusion injury.JHEP reports : innovation in hepatology · 2023Article
- Cardiovascular Brain Circuits.Circulation research · 2023Review
- Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells.Cardiovascular research · 2023Article
- ILC2-mediated immune crosstalk in chronic (vascular) inflammation.Frontiers in immunology · 2023Review
- Genetic Analysis Reveals Different Mechanisms of IL-5 Involved in the Development of CAD in a Chinese Han Population.Oxidative medicine and cellular longevity · 2023Article
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17 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundInnate lymphoid cells type 2 (ILC2s) play critical homeostatic functions in peripheral tissues. ILC2s reside in perivascular niches and limit atherosclerosis development.
objectivesILC2s also reside in the pericardium but their role in postischemic injury is unknown.
methodsWe examined the role of ILC2 in a mouse model of myocardial infarction (MI), and compared mice with or without genetic deletion of ILC2. We determined infarct size using histology and heart function using echocardiography. We assessed cardiac ILC2 using flow cytometry and RNA sequencing. Based on these data, we devised a therapeutic strategy to activate ILC2 in mice with acute MI, using exogenous interleukin (IL)-2. We also assessed the ability of low-dose IL-2 to activate ILC2 in a double-blind randomized clinical trial of patients with acute coronary syndromes (ACS).
resultsWe found that ILC2 levels were increased in pericardial adipose tissue after experimental MI, and genetic ablation of ILC2 impeded the recovery of heart function. RNA sequencing revealed distinct transcript signatures in ILC2, and pointed to IL-2 axis as a major upstream regulator. Treatment of T-cell-deficient mice with IL-2 (to activate ILC2) significantly improved the recovery of heart function post-MI. Administration of low-dose IL-2 to patients with ACS led to activation of circulating ILC2, with significant increase in circulating IL-5, a prototypic ILC2-derived cytokine.
conclusionsILC2s promote cardiac healing and improve the recovery of heart function after MI in mice. Activation of ILC2 using low-dose IL-2 could be a novel therapeutic strategy to promote a reparative response after MI.
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