ArticleCirculation2025
Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination.
Article in Circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Evidence for Autoimmunity in the Pathogenesis of COVID-19-Induced Myocarditis.International journal of molecular sciences · 2026Article
- Acute myocarditis and rhabdomyositis after coronavirus disease 2019 messenger RNA vaccination and intensive training: a case report.Journal of medical case reports · 2026Article
- "Bridging the clinical, molecular and genetic perspectives on myocarditis in post-COVID-19 era".International journal of cardiology. Cardiovascular risk and prevention · 2026Review
- Article
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Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe COVID-19 pandemic, caused by SARS-CoV-2, has led to the first approval of mRNA vaccines in humans. By producing the full-length SARS-CoV-2 Spike protein, they induce protective antiviral immunity. Acute myopericarditis (AMP) development after vaccination has repeatedly been reported; however, the pathogenesis of this complication remains elusive.
methodsIn-depth phenotyping of peripheral blood T cells was undertaken in cohorts of patients who developed AMP after mRNA vaccination, patients hospitalized for severe COVID-19, and healthy subjects with no cardiac side effects after mRNA vaccine. Validation studies were carried out using an experimental model of cardiac inflammation, in which a shared epitope elicits functional responses in patients and mice and induces AMP.
resultsWe show that T cells from patients with AMP recognize vaccine-encoded Spike epitopes homologous to those of cardiac self-proteins. One of these epitopes, mimicking an amino acid sequence from a cardiomyocyte-expressed K
conclusionsAMP development after mRNA vaccines is mediated by distinct immune components, including molecular mimicry, T-cell receptor affinity, and, importantly, homing imprinting.
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