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Immune Profiling Identifies Inflammatory Signatures In Immune Checkpoint Inhibitor-related Myocarditis.

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Immune Profiling Identifies Inflammatory Signatures In Immune Checkpoint Inhibitor-related Myocarditis.

Related Experiment Video

Isolation and Identification of Extravascular Immune Cells of the Heart

Isolation and Identification of Extravascular Immune Cells of the Heart

Published on: August 23, 2018

Immune Profiling Identifies Inflammatory Signatures in Immune Checkpoint Inhibitor-Related Myocarditis.

Douglas Daoudlarian¹, Sarah Boughdad², Robin Bartolini¹

¹Centre Hospitalier Universitaire Vaudois (CHUV), University of Lausanne, Department of Medicine, Immunology and Allergy Service, Lausanne, Switzerland.

JACC. Cardiooncology

|June 17, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

Immune checkpoint inhibitor-associated myocarditis (ICI-My) shows a distinct inflammatory signature centered on IL-6 and chemokines. Conventional cardiac biomarkers are better for assessing ICI-My severity than single cytokines.

Keywords:

biomarkers immune checkpoint inhibitors myocarditis tocilizumab

Related Experiment Videos

Isolation and Identification of Extravascular Immune Cells of the Heart

Isolation and Identification of Extravascular Immune Cells of the Heart

Published on: August 23, 2018

Area of Science:

Immunology
Cardiology
Oncology

Background:

Immune checkpoint inhibitor-associated myocarditis (ICI-My) is a rare but serious adverse event.
There is a need for biomarkers to differentiate ICI-My from general immune activation by immune checkpoint inhibitors (ICIs).

Purpose of the Study:

To characterize the circulating inflammatory and cellular immune profiles in ICI-My.
To correlate these immune profiles with clinical severity.
To explore the potential of interleukin-6 receptor (IL-6R) blockade in refractory cases.

Main Methods:

Retrospective cohort study of 33 ICI-My patients and 68 ICI-treated controls.
Multiplex cytokine profiling and mass cytometry analyses were performed.
Eight steroid-refractory ICI-My patients were treated with tocilizumab compassionately.

Main Results:

ICI-My patients exhibited elevated circulating IL-6, chemokines (CCL3, CCL4, CCL5, CXCL9, CXCL10, CXCL13), and VEGF-A compared to controls.
Distinct cellular immune differences were observed, including altered neutrophil and T/B cell populations.
Conventional cardiac biomarkers (troponin T, BNP, AST, ALT) were more effective in distinguishing severe from non-severe ICI-My.

Conclusions:

Peripheral immune profiling reveals an IL-6 and chemokine-driven inflammatory signature specific to ICI-My.
Standard cardiac biomarkers are more reliable for assessing ICI-My severity.
IL-6R blockade with tocilizumab is feasible in selected steroid-refractory cases and warrants further investigation.