ArticleThe Journal of clinical investigation2003
IL-12 is required for differentiation of pathogenic CD8+ T cell effectors that cause myocarditis.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 108 citations in OpenAlex.
- Immune checkpoint inhibitor-induced myocarditis is dependent on CD8 T cell-derived TNF and TNFR2 signaling.The Journal of experimental medicine · 2026Article
- Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.Frontiers in immunology · 2026Review
- Targeting inflammation with chimeric antigen receptor macrophages using a signal switch.Nature biomedical engineering · 2025Article
- Preclinical mouse models of immune checkpoint inhibitor-associated myocarditis.Nature cardiovascular research · 2025Review
- Macrophage-derived SPP1 exacerbate myocardial injury by interacting with fibroblasts in viral myocarditis.Biology direct · 2025Article
- Integrated Metabolomics and Proteomics Analysis of the Myocardium in a Mouse Model of Acute Viral Myocarditis.Immunity, inflammation and disease · 2025Article
- Preclinical models of cardiotoxicity from immune checkpoint inhibitor therapy.Basic research in cardiology · 2025Review
- Altered colonic microflora and its metabolic profile in mice with acute viral myocarditis induced by coxsackievirus B3.Virology journal · 2024Article
- Recent advances in understanding the roles of T cells in atrial fibrillation.NPJ cardiovascular health · 2024Article
- Article
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- LncGBP9 knockdown alleviates myocardial inflammation and apoptosis in mice with acute viral myocarditis via suppressing NF-κB signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Cardiac myosin-specific autoimmune T cells contribute to immune-checkpoint-inhibitor-associated myocarditis.Cell reports · 2022Article
- Identification of Pathogenic Immune Cell Subsets Associated With Checkpoint Inhibitor-Induced Myocarditis.Circulation · 2022Article
- Knockdown of LncRNA MALAT1 Alleviates Coxsackievirus B3-Induced Acute Viral Myocarditis in Mice via Inhibiting Th17 Cells Differentiation.Inflammation · 2022Article
- Neutralization of interleukin-38 exacerbates coxsackievirus B3-induced acute myocarditis in mice.Virology journal · 2021Article
- Specialized transendothelial dendritic cells mediate thymic T-cell selection against blood-borne macromolecules.Nature communications · 2021Article
- Cytotoxic CD8Nature communications · 2021Article
- Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis.Journal of cellular and molecular medicine · 2020Article
- CD11b is involved in coxsackievirus B3-induced viral myocarditis in mice by inducing Th17 cells.Open life sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiac antigen-specific CD8(+) T cells are involved in the autoimmune component of human myocarditis. Here, we studied the differentiation and migration of pathogenic CD8(+) T cell effector cells in a new mouse model of autoimmune myocarditis. A transgenic mouse line was derived that expresses cardiac myocyte restricted membrane-bound ovalbumin (CMy-mOva). The endogenous adaptive immune system of CMy-mOva mice displays tolerance to ovalbumin. Adoptive transfer of naive CD8(+) T cells from the ovalbumin-specific T cell receptor-transgenic (TCR-transgenic) OT-I strain induces myocarditis in CMy-mOva mice only after subsequent inoculation with ovalbumin-expressing vesicular stomatitis virus (VSV-Ova). OT-I effector T cells derived in vitro in the presence or absence of IL-12 were adoptively transferred into CMy-mOva mice, and the consequences were compared. Although IL-12 was not required for the generation of cytolytic and IFN-gamma-producing effector T cells, only effectors primed in the presence of IL-12 infiltrated CMy-mOva hearts in significant numbers, causing lethal myocarditis. Furthermore, analysis of OT-I effectors collected from a mediastinal draining lymph node indicated that only effectors primed in vitro in the presence of IL-12 proliferated in vivo. These data demonstrate the importance of IL-12 in the differentiation of pathogenic CD8(+) T cells that can cause myocarditis.
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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.