ArticleThe Journal of experimental medicine2026
Immune checkpoint inhibitor-induced myocarditis is dependent on CD8 T cell-derived TNF and TNFR2 signaling.
Article in The Journal of experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A narrative review of immune checkpoint inhibitor-related cardiotoxicity in lung cancer: mechanisms, risk stratification, and clinical management.Journal of thoracic disease · 2026Review
- FUNDC1-mediated mitochondrial quality control protects against immune checkpoint inhibitor-associated cardiac injury.Immunologic research · 2026Article
- Cardiac-targeting peptide-modified Prussian blue nanozymes loaded with Astragaloside IV for efficient ICI-myocarditis therapy.Materials today. Bio · 2026Article
- Immune checkpoint inhibitor-induced cardiotoxicity: from immune mechanisms to clinical surveillance and targeted therapies.Frontiers in cardiovascular medicine · 2026Review
- Advancing precision cardio-oncology: multimodal surveillance and stratified management of immunotherapy-induced cardiovascular toxicity.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Immune checkpoint inhibitors (ICIs) improve cancer survival but can trigger immune-related adverse events. Among these, fulminant myocarditis is an often fatal complication with limited therapies. We developed a mouse model employing cardiomyocyte-restricted antigen expression to define how ICIs drive cardiac autoimmunity. Combined cytotoxic T cell antigen-4 (αCTLA-4) and programmed death-1 (αPD-1) blockade uniquely induced robust expansion of antigen-specific CD8 T cells, myocardial inflammation, and lethal arrhythmias. PD-1 blockade alone permitted the priming and effector differentiation of naive autoreactive CD8 T cells, whereas concomitant CTLA-4 inhibition amplified cardiac pathology. Unexpectedly, myocardial injury was independent of perforin-mediated cytotoxicity but critically depended on T cell-derived TNF, which promoted myeloid recruitment, cytokine production, and arrhythmogenesis. Genetic ablation of CD8 T cell-derived tumor necrosis factor (TNF) or TNF receptor 2 (TNFR2) blockade prevented cardiotoxicity while preserving antitumor efficacy. These findings establish a TNF-TNFR2-driven inflammatory circuit downstream of autoreactive CD8 T cells as a central mechanism of ICI myocarditis and a strategy to uncouple cardiotoxicity from immunotherapy benefits.
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Registered trials
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