ArticleEuropean journal of immunology2016
Pathogenic IL-23 signaling is required to initiate GM-CSF-driven autoimmune myocarditis in mice.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- IL-1-Activated Inflammatory Cardiac Fibroblasts Exacerbate Acute Coxsackievirus B3 Myocarditis.JACC. Basic to translational science · 2026Article
- Proteomics analysis of aqueous and vitreous humor in uveitis: a systematic literature review.Clinical proteomics · 2025Review
- Review
- The distinct functions of MIF in inflammatory cardiomyopathy.Frontiers in immunology · 2025Review
- Innate and adaptive immunity in acute myocarditis.International journal of cardiology · 2024Review
- Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries.Journal of clinical medicine · 2023Review
- Who Knew? Dopamine Transporter Activity Is Critical in Innate and Adaptive Immune Responses.Cells · 2023Article
- Cardiac myosin-specific autoimmune T cells contribute to immune-checkpoint-inhibitor-associated myocarditis.Cell reports · 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
- Myocarditis and inflammatory cardiomyopathy: current evidence and future directions.Nature reviews. Cardiology · 2021Review
- Transcriptomic Analysis of Inflammatory Cardiomyopathy Identifies Molecular Signatures of Disease and InformsFrontiers in immunology · 2021Article
- Depletion of langerinImmunology · 2020Article
- Proteomic analysis of intermediate uveitis suggests myeloid cell recruitment and implicates IL-23 as a therapeutic target.American journal of ophthalmology case reports · 2020Article
- IL-23 in arthritic and inflammatory pain development in mice.Arthritis research & therapy · 2020Article
- GM-CSF in inflammation.The Journal of experimental medicine · 2020Review
- Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges.Frontiers in pharmacology · 2020Review
- Growth Factors as Immunotherapeutic Targets in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- Oncogenic kinase inhibition limits Batf3-dependent dendritic cell development and antitumor immunity.The Journal of experimental medicine · 2019Article
- Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease.International journal of molecular sciences · 2019Review
- Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesis.Basic research in cardiology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Using a mouse model of experimental autoimmune myocarditis (EAM), we showed for the first time that IL-23 stimulation of CD4(+) T cells is required only briefly at the initiation of GM-CFS-dependent cardiac autoimmunity. IL-23 signal, acting as a switch, turns on pathogenicity of CD4(+) T cells, and becomes dispensable once autoreactivity is established. Il23a(-/-) mice failed to mount an efficient Th17 response to immunization, and were protected from myocarditis. However, remarkably, transient IL-23 stimulation ex vivo fully restored pathogenicity in otherwise nonpathogenic CD4(+) T cells raised from Il23a(-/-) donors. Thus, IL-23 may no longer be necessary to uphold inflammation in established autoimmune diseases. In addition, we demonstrated that IL-23-induced GM-CSF mediates the pathogenicity of CD4(+) T cells in EAM. The neutralization of GM-CSF abrogated cardiac inflammation. However, sustained IL-23 signaling is required to maintain IL-17A production in CD4(+) T cells. Despite inducing inflammation in Il23a(-/-) recipients comparable to wild-type (WT), autoreactive CD4(+) T cells downregulated IL-17A production without persistent IL-23 signaling. This divergence on the controls of GM-CSF-dependent pathogenicity on one side and IL-17A production on the other side may contribute to the discrepant efficacies of anti-IL-23 therapy in different autoimmune diseases.
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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.