ArticleESC heart failure2020
Characterization of dendritic cells in human and experimental myocarditis.
Article in ESC heart failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Biopsy-proven myocarditis: peripheral immunophenotypes correlate with histology, etiology, immunosuppressive therapy.Journal of translational autoimmunity · 2026Article
- The effect of cuproptosis-related gene Atox1 on cardiac hypertrophy in heart failure was investigated based on bioinformatics analysis.Scientific reports · 2025Article
- Coronin 1 deficiency protects from the development of autoimmune myocarditis by reducing CD4+ T cells.ESC heart failure · 2025Article
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Uncovering dendritic cell specific biomarkers for diagnosis and prognosis of cardiomyopathy using single cell RNA sequencing and comprehensive bioinformatics analysis.Scientific reports · 2025Article
- The immune checkpoint regulator CD40 potentiates myocardial inflammation.Nature cardiovascular research · 2025Article
- The Immune System, An Arrow into the Heart. Principles of Cardioimmunology, An Emerging Branch in Medicine.Current vascular pharmacology · 2025Review
- Review
- Lab-on-a-chip models of cardiac inflammation.Biomicrofluidics · 2024Review
- Activation of ETAR and ETBR in myocardial tissue characterizes heart failure induced by experimental autoimmune myocarditis.BMC cardiovascular disorders · 2024Article
- High placental expression of FLT1, LEP, PHYHIP and IL3RA - In persons of African ancestry with severe preeclampsia.Placenta · 2023Article
- Role of monocytes and dendritic cells in cardiac reverse remodelling after cardiac resynchronization therapy.BMC cardiovascular disorders · 2023Article
- Emerging Roles for Dendritic Cells in Heart Failure.Biomolecules · 2023Review
- Integrated Single-Cell and RNA Sequencing Analysis Identifies Key Immune Cell and Dendritic Cells Associated Genes Participated in Myocarditis.Journal of immunology research · 2022Article
- In the Acute Phase ofFrontiers in immunology · 2022Article
- Indoleamine 2,3-dioxygenase 1 limits hepatic inflammatory cells recruitment and promotes bile duct ligation-induced liver fibrosis.Cell death & disease · 2021Article
- Characterization of dendritic cells in human and experimental myocarditis.ESC heart failure · 2020Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
aimsDendritic cells (DCs) are central mediators of adaptive immunity, and there is growing evidence of their role in myocardial inflammatory disease. We hypothesized that plasmacytoid and myeloid DCs are involved in the mechanisms of myocarditis and analysed these two main subtypes in human myocarditis subjects, as well as in a murine model of experimental autoimmune myocarditis (EAM). METHODS AND
resultsCirculating DCs were analysed by flow cytometry in patients with acute myocarditis, dilated cardiomyopathy, and controls. Myocardial biopsies were immunostained for the presence of DCs and compared with non-diseased controls. In a mouse model of acute myocarditis induced through synthetic cardiac myosine peptide injection, effects of immunomodulation including DC inhibition through MCS-18 versus placebo treatment were tested at the peak of inflammation (Day 21), as well as 1 week later (partial recovery). Circulatory pDCs and mDCs were significantly reduced in myocarditis patients compared with controls (P < 0.01 for both) and remained so even after 6 months of follow-up. Human myocarditis biopsies showed accumulation of pDCs (two-fold CD304+/three-fold CD123+, all P < 0.05) compared with controls. Myocardial pDCs and mDCs accumulated in EAM (P for both <0.0001). MCS-18 treatment reduced pDC levels (P = 0.009), reduced myocardial inflammation (myocarditis score reduction from 2.6 to 1.8, P = 0.026), and improved ejection fraction (P = 0.03) in EAM at Day 21 (peak of inflammation). This effect was not observed during the partial recovery of inflammation on Day 28.
conclusionsCirculating DCs are reduced in human myocarditis and accumulate in the inflamed myocardium. MCS-18 treatment reduces DCs in EAM, leading to amelioration of inflammation and left ventricular remodelling during the acute phase of myocarditis. Our data further elucidate the role of DCs and their specific subsets in acute inflammatory cardiomyopathies.
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