{"id":"85ff58ac9d5b","type":"article","url":"https://hartvaat.nl/2026/01/07/cxcr6-t-cellen-veroorzaken-immuuncheckpointremmer-myocarditis/","title":"CXCR6+ T-cellen veroorzaken immuuncheckpointremmer-myocarditis","title_en":"CXCR6+ T Cells Drive Immune Checkpoint Inhibitor Myocarditis","category":"algemeen","category_label":"Algemeen","professions":["cardioloog","internist"],"tags":["inflammatie","inflammatoire-cardiomyopathie","myocarditis"],"journal":"Circulation","doi":"https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.076976","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.076976","authors":[],"significance":8,"published":"2026-01-07","source_date":"2026-01-07","image":"","kennis":["https://hartvaat.nl/kennis/cardiometabool/hart-en-kanker-cardio-oncologie/"],"congress":"","summary_en":"This study identified CXCR6+ T cells as key drivers of immune checkpoint inhibitor-associated myocarditis, particularly with combination ICI therapy including anti-LAG-3 agents. The mechanistic insight may guide future prevention and treatment strategies for this serious complication.","created":"2026-07-03T10:25:35Z","updated":"2026-07-03T13:24:58Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Myocarditis is een ernstige complicatie van immuuncheckpointremmers, vooral bij combinatietherapie met relatlimab (anti-LAG-3). Dit onderzoek identificeert CXCR6+ T-cellen als drijvende kracht achter ICI-geïnduceerde myocarditis.","abstract_original":"BACKGROUND:Myocarditis is a severe complication of immune checkpoint inhibitors (ICIs). The major risk factor for ICI myocarditis is the use of combination ICI treatment, especially when relatlimab, a novel anti–LAG-3 (lymphocyte-activation gene 3) antibody, is combined with anti–PD-1 (programmed cell death protein 1) therapy. Although pathogenic T cells are necessary for ICI myocarditis, the specific signaling and T-cell populations that drive cardiac infiltration have not been fully elucidated, especially in setting of anti–LAG-3/PD-1 treatment.METHODS:We used VigiBase, an international pharmacovigilance database, to assess the risk of myocarditis with anti–LAG-3 compared with other ICI treatment regimens. We identified a mouse model of LAG-3/PD-1–associated ICI myocarditis through genetic deletion of immune checkpoints LAG-3 and PD-1 (Lag3-/-, Pdcd1-/-mice) and performed rigorous cardiac phenotyping using histology, flow cytometry, electrocardiography, single-cell RNA sequencing, an"}