CXCR6 + T Cells Drive Immune Checkpoint Inhibitor Myocarditis
Authors' conclusion
Our findings suggest that ICI myocarditis is driven by an expansion of CXCR6+ T cells and identifies CXCR6 as a putative therapeutic target for this highly morbid condition.
Study context
- Population
- ICI myocarditis: VigiBase pharmacovigilance reports and Lag3-/-, Pdcd1-/- mouse model
- Comparison
- Anti-LAG-3 combination vs other ICI regimens (VigiBase); anti-CXCR6 antibody treatment in Lag3-/-, Pdcd1-/- mice
Methodological detailspharmacovigilance database analysis, mouse model (Lag3-/-, Pdcd1-/-)
- Pharmacovigilance database analysis
- Mouse model (Lag3-/-, Pdcd1-/-)
Main finding
As reported in the abstract
- Increased risk of myocarditis with anti-LAG-3 combination treatment clinically
- Lag3-/-, Pdcd1-/- mice developed severe cardiac inflammation with increased cardiac macrophages and clonal T cells, spontaneous arrhythmias and premature death by 6 to 8 weeks
- CXCR6 a key marker of activated cardiac T cells (heterogenous: Gzmk, Gzmb, Cd4, actively dividing clusters), with analogous signals in other preclinical models and patient data
- CXCL16 upregulated in cardiac macrophages
- Anti-CXCR6 antibody prevented premature lethality, attenuated arrhythmias and reduced histological severity of myocarditis
Original publication
CXCR6 + T Cells Drive Immune Checkpoint Inhibitor Myocarditis. Circulation. Published 7 January 2026. doi:10.
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