Cardio-oncology & otherCohort study
Immune Profiling Identifies Inflammatory Signatures in Immune Checkpoint Inhibitor–Related Myocarditis
- Retrospective cohort study
- single-centre
Authors' conclusion
Peripheral immune profiling identifies an IL-6-centered and chemokine-centered inflammatory signature in ICI-My beyond background ICI exposure. Conventional cardiac biomarkers remain more informative than single cytokines for severity assessment in this cohort.
Study context
- Population
- Patients treated with immune checkpoint inhibitors, single centre, January 2018 to June 2024mass cytometry 16 vs 72
- Participants
- 33 vs 68
- Exposure
- ICI-My vs ICI-treated patients without myocarditis
- ICI-Myn = 33
- ICI-treated controlsn = 68reference
Main finding
As reported in the abstract
Circulating inflammatory and cellular immune profile
- ICI-My associated with higher circulating IL-6, CCL3, CCL4, CCL5, CXCL9, CXCL10, CXCL13 and VEGF-A vs ICI-treated controls
- Mass cytometry: higher immature neutrophils and activated HLA-DR+CD38+ CD4+ and CD8+ T cells, lower CXCR5+ memory B- and T-cell populations, contraction of switched and unswitched memory B-cell compartments, lower CXCR3 across memory T-cell subsets
- No clear systemic complement activation signal
Observational data: associations, not effects.
Further findings
Discrimination of severe vs nonsevere myocarditis
- High-sensitivity troponin T, NT-proBNP, AST and ALT discriminated severity more consistently than individual cytokines
Tocilizumab in steroid-refractory cases (compassionate use, n = 8)
- Tocilizumab administration feasible; uncontrolled series cannot establish efficacy
Original publication
Immune Profiling Identifies Inflammatory Signatures in Immune Checkpoint Inhibitor–Related Myocarditis. JACC CardioOncol. doi:10.1016/j.jaccao.2026.04.008
Summarised from the published abstract; every number is checked against it