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Updated: May 19, 2026

Isolation and Identification of Extravascular Immune Cells of the Heart
Published on: August 23, 2018
The inflammatory fingerprint reveals immune cell populations associated with disease activity in cardiac sarcoidosis
Tobias Harm1, Stella E Autenrieth2, Katharina Mezger1
1Department of Cardiology and Angiology, University Hospital Tübingen, Otfried-Müller-Straße 10, 72076, Tübingen, Germany.
Insights
Cardiac sarcoidosis (CS) involves distinct immune cell changes. Understanding these inflammatory fingerprints helps identify patients who may benefit from immunosuppressive therapy for better outcomes.
Area of Science:
- Immunology
- Cardiology
- Systemic inflammatory diseases
Background:
- Sarcoidosis is a systemic inflammatory disease.
- Cardiac involvement in sarcoidosis increases adverse event risk.
- Pathophysiology of myocardial inflammation and fibrosis in sarcoidosis is not fully understood.
Purpose of the Study:
- Characterize the immune response in cardiac sarcoidosis (CS).
- Identify immune signatures associated with disease activity and prognosis.
- Understand the pathophysiology of CS.
Main Methods:
- Prospective enrollment of 26 patients with biopsy-proven sarcoidosis.
- Evaluation of suspected CS using hybrid cardiac PET/MR imaging.
- Analysis of peripheral blood from active CS, chronic CS, extracardiac sarcoidosis, and healthy controls via spectral flow cytometry and immunoassay.
Main Results:
- Identified 56 characteristic immune cell populations in CS patients.
- Revealed distinct immunophenotypic differences between CS patients, extracardiac sarcoidosis, and healthy controls.
- Observed aberrant cytokine/chemokine expression and shifts in lymphocytes, innate immune cells, and monocyte subsets in CS.
Conclusions:
- Comprehensive immune profiling reveals changes in immune cell populations linked to CS.
- Findings offer insights into CS pathophysiology.
- Potential for improved patient stratification for targeted immunosuppressive therapy.
Objective:
Sarcoidosis is a systemic granulomatous inflammatory disease and patients with cardiac involvement are at increased risk of adverse events. Pathophysiologic processes leading to myocardial inflammation and fibrosis are yet to be determined. Therefore, characterization of the immune response leading to enhanced disease activity and portending poor prognosis of patients with cardiac sarcoidosis (CS) is crucial.
Methods:
Twenty-six patients with biopsy-proven sarcoidosis were prospectively enrolled for evaluation of suspected CS and disease activity was determined by hybrid cardiac PET/MR imaging. We then analyzed the peripheral blood of individuals with active CS (aCS), chronic CS (cCS), extracardiac sarcoidosis (noCS), and healthy controls using a 36-color spectral flow cytometry and immunoassay panel.
Results:
Analysis of the inflammatory fingerprint in patients with CS uncovered 56 characteristic immune cell populations. Immunophenotyping of the inflammatory cells revealed distinctive differences between healthy individuals and patients with sarcoidosis. Further, the abundance of the cell populations was associated with cardiac manifestation and disease activity. A critical shift of lymphocytes, innate immune cells, and monocyte subsets occurred in patients with CS compared to extracardiac sarcoidosis and healthy individuals. In addition, cytokine/chemokine expression was aberrant in patients with CS and may contribute to the cardiac pathophysiology of sarcoidosis.
Conclusions:
Comprehensive characterization of the inflammatory fingerprint reveals changes in frequency and phenotype of several immune cell populations associated with cardiac sarcoidosis. Our results may add further knowledge to the pathophysiology of cardiac sarcoidosis, allowing a better stratification of patients with high disease activity who seem to benefit most from immunosuppressive therapy.
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