ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Cardiac-targeting peptide-modified Prussian blue nanozymes loaded with Astragaloside IV for efficient ICI-myocarditis therapy.Materials today. Bio · 2026Article
- Pathological mechanisms and treatment strategies for immune checkpoint inhibitor-associated myocarditis: insights from single-cell sequencing.Basic research in cardiology · 2026Review
- Immune checkpoint inhibition and heart injury: molecular mechanisms and clinical challenges.ESC heart failure · 2026Review
- Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.Frontiers in immunology · 2026Review
- Single-cell transcriptomic insights into the immune heterogeneity of immune checkpoint inhibitors related organ toxicities.Frontiers in immunology · 2026Review
- Understanding immune checkpoint inhibitors-related myocarditis: Mechanisms and targeted therapeutic pathways.Theranostics · 2026Review
- From tumor immunotherapy to myocardial injury: A mechanistic discussion of immune checkpoint inhibitor‑related myocarditis (Review).Molecular medicine reports · 2025Review
- Neutrophils in Myocarditis: A Focus on the Secretory and Phagocytotic Functions.Reviews in cardiovascular medicine · 2025Review
- Development of peripheral biomarker-based prognostic nomograms for short-term and long-term survival in immune checkpoint inhibitor-associated myocarditis.Cardiovascular diagnosis and therapy · 2025Article
- Dynamic single-cell transcriptomic reveals the cellular heterogeneity and a novel fibroblast subpopulation in laryngotracheal stenosis.Biology direct · 2025Article
- Targeting persistently activated inflammatory microenvironment to promote chronic wound healing.Frontiers in immunology · 2025Review
- PD-1 inhibition disrupts collagen homeostasis and aggravates cardiac dysfunction through endothelial-fibroblast crosstalk and EndMT.Frontiers in pharmacology · 2025Article
- The role of immune checkpoints PD-1 and CTLA-4 in cardiovascular complications leading to heart failure.Frontiers in immunology · 2025Review
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Mesenchymal stromal cells alleviate APAP-induced liver injury via extracellular vesicle-mediated regulation of the miR-186-5p/CXCL1 axis.Stem cell research & therapy · 2024Article
- Article
- Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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21 authors.
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Abstract
The risk for suffering immune checkpoint inhibitors (ICIs)-associated myocarditis increases in patients with pre-existing conditions and the mechanisms remain to be clarified. Spatial transcriptomics, single-cell RNA sequencing, and flow cytometry are used to decipher how anti-cytotoxic T lymphocyte antigen-4 m2a antibody (anti-CTLA-4 m2a antibody) aggravated cardiac injury in experimental autoimmune myocarditis (EAM) mice. It is found that anti-CTLA-4 m2a antibody increases cardiac fibroblast-derived C-X-C motif chemokine ligand 1 (Cxcl1), which promots neutrophil infiltration to the myocarditic zones (MZs) of EAM mice via enhanced Cxcl1-Cxcr2 chemotaxis. It is identified that the C-C motif chemokine ligand 5 (Ccl5)-neutrophil subpopulation is responsible for high activity of cytokine production, adaptive immune response, NF-κB signaling, and cellular response to interferon-gamma and that the Ccl5-neutrophil subpopulation and its-associated proinflammatory cytokines/chemokines promoted macrophage (Mφ) polarization to M1 Mφ. These altered infiltrating landscape and phenotypic switch of immune cells, and proinflammatory factors synergistically aggravated anti-CTLA-4 m2a antibody-induced cardiac injury in EAM mice. Neutralizing neutrophils, Cxcl1, and applying Cxcr2 antagonist dramatically alleviates anti-CTLA-4 m2a antibody-induced leukocyte infiltration, cardiac fibrosis, and dysfunction. It is suggested that Ccl5-neutrophil subpopulation plays a critical role in aggravating anti-CTLA-4 m2a antibody-induced cardiac injury in EAM mice. This data may provide a strategic rational for preventing/curing ICIs-associated myocarditis.
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