Investigating Mechanisms of Immunotherapy-Induced (ICI) Myocarditis

Immune checkpoint inhibitor (ICI) myocarditis is a rare but potentially fatal inflammatory heart disease that can occur as a complication of cancer immunotherapy. While immune checkpoint inhibitors have transformed cancer care, severe cardiovascular toxicities remain difficult to predict and treat, often limiting access to life-saving therapy for patients with cancer.

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Our lab investigates the immune and tissue-specific mechanisms driving ICI myocarditis using integrated translational approaches spanning human patient biospecimens, multi-omics profiling, and mechanistic experimental models. We combine single-cell and spatial transcriptomics, TCR sequencing, CyTOF, plasma cell-free RNA profiling, and human iPSC-based cardiac models with mouse models of disease to identify pathogenic immune cell states, antigen-specific T-cell responses, and fibroblast–immune cell signaling pathways that contribute to myocardial injury.

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A major focus of the lab is developing tumor-conscious therapeutic strategies that reduce cardiac inflammation while preserving the anti-tumor immune responses critical for effective cancer treatment. Through close collaboration with investigators across cardiology, oncology, immunology, and bioengineering at Stanford, we aim to translate mechanistic discoveries into new biomarkers and targeted therapies for patients with inflammatory cardiovascular disease.

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Funding Sources: NHLBI R01, NHLBI R03, AHA Transformational Project Award