A cross-species study links immune checkpoint inhibitor-associated myocarditis to a CD74-high antigen-presenting myeloid state enriched for interferon-gamma and STAT1 signaling. Researchers combined human transcriptomic datasets with single-cell cardiac profiling and then validated mechanism in a murine anti-PD-1 myocarditis model. In patients and in the mouse model, CD74 and MHC class II-related programs co-elevated in disease-associated myeloid cells and tracked with heart tissue damage and fibrosis. The team also tested intervention using an anti-CD74 antibody in the anti-PD-1 model, reporting reduced myocardial injury. The finding provides a clearer targetable myeloid pathway for managing a rare but high-risk adverse effect, while sharpening biomarker efforts that could improve risk stratification in future immunotherapy studies.