Expansion of Pathogenic Cardiac Macrophages in Immune Checkpoint Inhibitor Myocarditis
Authors' conclusion
These data demonstrate that ICI myocarditis is associated with the expansion of a specific population of IFN-γ-induced inflammatory macrophages
Study context
- Population
- Murine ICI myocarditis model (Ctla4+/-Pdcd1-/- mice); patients with ICI myocarditis
- Outcome
- Cardiac immune landscape in ICI myocarditis
Methodological detailsmurine ICI myocarditis model (Ctla4+/-Pdcd1-/- mice), single-cell RNA-sequencing, antibody neutralization studies
- Murine ICI myocarditis model (Ctla4+/-Pdcd1-/- mice)
- Single-cell RNA-sequencing
- Antibody neutralization studies
Main finding
As reported in the abstract
- Marked increases in CCR2+ monocyte-derived macrophages and CD8+ T-cells
- Enrichment in an inflammatory CCR2+ macrophage subpopulation highly expressing Cxcl9, Cxcl10, Gbp2b and Fcgr4, originating from CCR2+ monocytes
- Similar macrophage population expressing CXCL9, CXCL10 and CD16α expanded in patients with ICI myocarditis
- In silico prediction: T-cell–Cxcl9+Cxcl10+ macrophage interactions via IFN-γ and CXCR3 signaling
- Depleting CD8+ T-cells or macrophages and IFN-γ blockade blunted Cxcl9+Cxcl10+ macrophage expansion and attenuated myocarditis
Original publication
Expansion of Pathogenic Cardiac Macrophages in Immune Checkpoint Inhibitor Myocarditis. Circulation. Published 25 September 2023. doi:10.
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