Targeting CXCR6: A New Therapeutic Frontier in Immune Checkpoint Inhibitor-Induced Myocarditis

Introduction: The Growing Challenge of ICI-Induced Cardiotoxicity

The landscape of oncology has been fundamentally transformed by the advent of immune checkpoint inhibitors (ICIs). By blocking inhibitory pathways such as programmed cell death protein 1 (PD-1), its ligand (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), these therapies have significantly improved survival across various malignancies. However, the non-specific activation of the immune system often leads to immune-related adverse events (irAEs). Among these, ICI-induced myocarditis is particularly feared. Although it occurs in less than 1% of patients, it carries a high mortality rate—often exceeding 40% to 50%—and frequently presents as a fulminant clinical course characterized by arrhythmias, heart failure, and cardiogenic shock.

The Emergence of LAG-3 Inhibition