Researchers at Stanford Medicine identified a possible biological explanation for why a very small number of people develop myocarditis after mRNA COVID-19 vaccination. The study focused on immune system signaling pathways involving CXCL10 and interferon-gamma (IFN-γ).
The researchers found that certain immune cells released high levels of CXCL10 after exposure to mRNA vaccines. That signal then activated T cells, increasing IFN-γ production and amplifying inflammation that, in rare cases, could affect heart tissue.
Importantly, the study emphasized that myocarditis after mRNA vaccination remains uncommon and is usually mild to moderate, with most patients recovering fully. The researchers and health authorities also noted that COVID-19 infection itself carries a higher risk of myocarditis than vaccination.
In laboratory and animal models, blocking CXCL10 and IFN-γ reduced inflammatory damage while preserving much of the immune response, suggesting a possible path for future treatments or safer vaccine designs.
The work was published in Science Translational Medicine and led by researchers including Joseph Wu and Xu Cao.