Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.
J, H., X, X., Y, J., L, Q., H, Y., W, G., & C, L. (2026). Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1752354
J H, X X, Y J, L Q, H Y, W G, et al. Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.. Frontiers in immunology. 2026; doi: 10.3389/fimmu.2026.1752354
J H, X X, Y J, et al. Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.[J]. Frontiers in immunology. 2026. DOI: 10.3389/fimmu.2026.1752354.
@article{j2026,
author = {Huang J and Xu X and Jin Y and Qiao L and Yu H and Gao W and Li C},
title = {Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.},
journal = {Frontiers in immunology},
year = {2026},
doi = {10.3389/fimmu.2026.1752354},
note = {PMID: 42327747},
}
TY - JOUR AU - Huang J AU - Xu X AU - Jin Y AU - Qiao L AU - Yu H AU - Gao W AU - Li C TI - Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk. T2 - Frontiers in immunology PY - 2026 DO - 10.3389/fimmu.2026.1752354 AN - PMID:42327747 ER -
Immune checkpoint inhibitors (ICIs) have transformed cancer therapy but can induce immune-related myocarditis (ICI-MC), a rare yet life-threatening toxicity. This review elucidates the cellular and molecular mechanisms underlying ICI-MC, integrating insights from T-cell dysregulation, innate immunity, and stromal interactions. Pathogenesis involves α-myosin-driven clonal expansion of cytotoxic CD8+ T cells, loss of regulatory subsets, and macrophage polarization toward M1 phenotypes via cGAS-STING and STAT1/NF-κB pathways. Crosstalk among macrophages, fibroblasts, endothelial cells, neutrophils, and B cells amplifies myocardial inflammation through chemokine and complement activation. A five-phase multicellular framework-baseline autoreactivity, checkpoint blockade, clonal expansion, effector execution, and inflammatory amplification-summarizes disease evolution. Candidate biomarkers and targeted therapies offer precision strategies to mitigate cardiotoxicity. Future single-cell and multi-omics studies are essential to refine diagnosis and develop cardioprotective interventions without compromising antitumor efficacy.