ArticleThe American journal of pathology2001
Experimental autoimmune myocarditis in A/J mice is an interleukin-4-dependent disease with a Th2 phenotype.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
80 citing papers in PubMed, 175 citations in OpenAlex.
- Article
- Cardiac Troponin I Antibodies Induce Cardiomyocyte Damage and Alter Cell Morphology.International journal of molecular sciences · 2025Article
- Coronin 1 deficiency protects from the development of autoimmune myocarditis by reducing CD4+ T cells.ESC heart failure · 2025Article
- Review
- The Role of the Immune System in Pathobiology and Therapy of Myocarditis: A Review.Biomedicines · 2024Review
- The inflammatory spectrum of cardiomyopathies.Frontiers in cardiovascular medicine · 2024Review
- The levels of circulating cytokines and risk of neuromyelitis optica spectrum disorder: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Article
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- Comparison of COVID-19 Vaccine-Associated Myocarditis and Viral Myocarditis Pathology.Vaccines · 2023Review
- COVID-19 Heart Lesions in Children: Clinical, Diagnostic and Immunological Changes.International journal of molecular sciences · 2023Review
- Buyang huanwu decoction (BYHWD) alleviates sepsis-induced myocardial injury by suppressing local immune cell infiltration and skewing M2-macrophage polarization.American journal of translational research · 2023Article
- Sex and gender differences in myocarditis and dilated cardiomyopathy: An update.Frontiers in cardiovascular medicine · 2023Review
- Circulating c-Met-Expressing Memory T Cells Define Cardiac Autoimmunity.Circulation · 2022Article
- Meeting the Challenges of Myocarditis: New Opportunities for Prevention, Detection, and Intervention-A Report from the 2021 National Heart, Lung, and Blood Institute Workshop.Journal of clinical medicine · 2022Article
- Estrogenic bias in T-Lymphocyte biology: Implications for cardiovascular disease.Pharmacological research · 2021Review
- Attenuated strain of CVB3 with a mutation in the CAR-interacting region protects against both myocarditis and pancreatitis.Scientific reports · 2021Article
- Sex Differences, Genetic and Environmental Influences on Dilated Cardiomyopathy.Journal of clinical medicine · 2021Review
- Sex differences in inflammation, redox biology, mitochondria and autoimmunity.Redox biology · 2020Review
- Autoimmunity in Acute Myocarditis: How Immunopathogenesis Steers New Directions for Diagnosis and Treatment.Current cardiology reports · 2020Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Myocarditis in humans is often associated with an autoimmune process in which cardiac myosin (CM) is a major autoantigen. Experimental autoimmune myocarditis (EAM) is induced in mice by immunization with CM. We found that EAM in A/J mice exhibits a Th2-like phenotype demonstrated by the histological picture of the heart lesions (eosinophils and giant cells) and by the humoral response (association of IgG1 response with disease and up-regulation of total IgE). Blocking interleukin (IL)-4 with anti-IL-4 monoclonal antibody (mAb) reduced the severity of EAM. This reduction in severity was associated with a shift from a Th2-like to a Th1-like phenotype represented by a reduction in CM-specific IgG1; an increase in CM-specific IgG2a; an abrogation of total IgE response; a decrease in IL-4, IL-5, and IL-13; as well as a dramatic increase in interferon (IFN)-gamma production in vitro. Based on the latter finding, we hypothesized that IFN-gamma limits disease. Indeed, IFN-gamma blockade with a mAb exacerbated disease. The ameliorating effect of IL-4 blockade was abrogated by co-administration of anti-IFN-gamma mAb. Thus, EAM represents a model of an organ-specific autoimmune disease associated with a Th2 phenotype, in which IL-4 promotes the disease and IFN-gamma limits it. Suppression of IFN-gamma represents at least one of the mechanisms by which IL-4 promotes EAM.
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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.