Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination
Authors' conclusion
AMP development after mRNA vaccines is mediated by distinct immune components, including molecular mimicry, T-cell receptor affinity, and, importantly, homing imprinting.
Study context
- Population
- Patients with acute myopericarditis after mRNA COVID-19 vaccination, patients hospitalized for severe COVID-19, and healthy vaccinated subjects; validation in an experimental mouse model of cardiac inflammationcohorts
- Comparison
- Acute myopericarditis (AMP) vs COVID-19 vs Healthy
- Outcome
- In-depth phenotyping of peripheral blood T cells; functional T-cell responses to vaccine-encoded Spike epitopes homologous to cardiac self-proteins
Methodological detailsexperimental model validation
- Experimental model validation
Main finding
As reported in the abstract
T-cell recognition of Spike epitopes homologous to cardiac self-proteins
- T cells from patients with AMP recognize vaccine-encoded Spike epitopes homologous to those of cardiac self-proteins
- One epitope, mimicking an amino acid sequence from a cardiomyocyte-expressed K+ channel, induced AMP in mice
- On functional responses to Kv2, AMP patients after mRNA vaccination — but not patients with COVID-19 — displayed an expanded pattern of cytokine production, similar to AMP mice and autoimmune myocarditis
- T-cell autoimmunity segregates to cardiotropic cMet (c-mesenchymal epithelial transition factor)-expressing T cells and is prevented by cMet inhibition
- Suggests heart homing imprinting, permitted by the unique mRNA vaccine biodistribution, is required for AMP development
Original publication
Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination. Circulation. Published 30 October 2025. doi:10.
Summarised from the published abstract; every number is checked against it