ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- Cardiac Involvement in Eosinophilic Granulomatosis with Polyangiitis.Current cardiology reports · 2025Review
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Differential roles of eosinophils in cardiovascular disease.Nature reviews. Cardiology · 2025Review
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- Review
- Eosinophilic Myocarditis: From Bench to Bedside.Biomedicines · 2024Review
- Article
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- COVID-19 Heart Lesions in Children: Clinical, Diagnostic and Immunological Changes.International journal of molecular sciences · 2023Review
- GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation.Blood advances · 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
- Multimarker profiling identifies protective and harmful immune processes in heart failure: findings from BIOSTAT-CHF.Cardiovascular research · 2022Article
- IFNγ and GM-CSF control complementary differentiation programs in the monocyte-to-phagocyte transition during neuroinflammation.Nature immunology · 2022Article
- The Roles of Cardiac Fibroblasts and Endothelial Cells in Myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Diagnosis and treatment of eosinophilic myocarditis.Journal of translational autoimmunity · 2021Review
- Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis.International journal of molecular sciences · 2020Review
- Autoimmunity in Acute Myocarditis: How Immunopathogenesis Steers New Directions for Diagnosis and Treatment.Current cardiology reports · 2020Review
- Heart disease in a mutant mouse model of spontaneous eosinophilic myocarditis maps to three loci.BMC genomics · 2019Article
- Myocarditis in Humans and in Experimental Animal Models.Frontiers in cardiovascular medicine · 2019Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
Abstract
CD4(+) T cells play a central role in inflammatory heart disease, implicating a cytokine product associated with Th cell effector function as a necessary mediator of this pathophysiology. IFN-γ-deficient mice developed severe experimental autoimmune myocarditis (EAM), in which mice are immunized with cardiac myosin peptide, whereas IL-17A-deficient mice were protected from progression to dilated cardiomyopathy. We generated IFN-γ(-/-)IL-17A(-/-) mice to assess whether IL-17 signaling was responsible for the severe EAM of IFN-γ(-/-) mice. Surprisingly, IFN-γ(-/-)IL-17A(-/-) mice developed a rapidly fatal EAM. Eosinophils constituted a third of infiltrating leukocytes, qualifying this disease as eosinophilic myocarditis. We found increased cardiac production of CCL11/eotaxin, as well as Th2 deviation, among heart-infiltrating CD4(+) cells. Ablation of eosinophil development improved survival of IFN-γ(-/-)IL-17A(-/-) mice, demonstrating the necessity of eosinophils in fatal heart failure. The severe and rapidly fatal autoimmune inflammation that developed in the combined absence of IFN-γ and IL-17A constitutes a novel model of eosinophilic heart disease in humans. This is also, to our knowledge, the first demonstration that eosinophils have the capacity to act as necessary mediators of morbidity in an autoimmune process.
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What OpenQuestion holds
Registered trials
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.