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Updated: Dec 25, 2025

Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
Macrophages represent the major pool of IL-7Rα expressing cells in patients with myocarditis
Natalia Kubin1, Manfred Richter1, Bedriye Sen-Hild2
1Department of Cardiac Surgery, Kerckhoff-Clinic, Benekestrasse 2-8, Bad Nauheim 61231, Germany.
Abstract:
Myocarditis is characterized by infiltration and activation of cytokine as well as chemokine receptors frequently producing heart failure. Causes are often infections triggering inflammatory and immune responses but these initial lines of defense might be finally disastrous. To identify mediators we screened various receptors by confocal microscopy and identified cardiac interleukin-7 (IL-7) receptor-α (IL-7Rα) expressing cells in patients with myocarditis. IL-7Rα+ cells were analyzed by markers for leukocytes (CD45), B cells (CD19), T cells (CD3, CD4, CD8) and macrophages (CD68, CD163, CD206). Immune cells were hardly detected in controls. In patients with myocarditis main inflammatory populations consisted of macrophages and T cells. B cells were hardly present. 90% of CD68+ macrophages but less than 20% of CD3+ T cells were IL-7Rα+. This was surprising since T and B lymphocytes are generally regarded as the major IL-7Rα+ cells. Since IL-7 acts as a chemokine, the expression of its receptor might orchestrate cardiac macrophage infiltration. In contrast, consumption of IL-7 by IL-7Rα+ cardiac macrophages might potentially prevent a certain overshooting immune reaction and sepsis by reducing proliferation and survival of lymphocytes. Our data suggest a participation of IL-7Rα+ macrophages in the development of myocarditis and heart failure.
Insights
Myocarditis involves cardiac interleukin-7 receptor-alpha (IL-7Rα) expressing macrophages, not just T cells. These IL-7Rα+ macrophages may influence heart failure development.
Area of Science:
- Immunology
- Cardiology
- Molecular Biology
Background:
- Myocarditis, often infection-induced, involves inflammatory responses and can lead to heart failure.
- Cytokine and chemokine receptors play a role in myocarditis pathogenesis.
- Interleukin-7 (IL-7) signaling is crucial for lymphocyte development and survival.
Purpose of the Study:
- To identify specific immune cell receptor mediators involved in myocarditis.
- To investigate the role of interleukin-7 receptor-alpha (IL-7Rα) in cardiac inflammation during myocarditis.
Main Methods:
- Confocal microscopy was used to screen various receptors in cardiac tissue from myocarditis patients.
- Immunohistochemical analysis identified IL-7Rα expressing cells and characterized them using leukocyte, B cell, T cell, and macrophage markers.
Main Results:
- Cardiac cells expressing IL-7Rα were identified in myocarditis patients, with immune cells being scarce in controls.
- Macrophages (CD68+) and T cells (CD3+) were the main inflammatory populations in myocarditis.
- A high percentage of macrophages (90%) expressed IL-7Rα, while fewer T cells (less than 20%) did.
Conclusions:
- The study identified IL-7Rα+ macrophages as a significant component of cardiac inflammation in myocarditis.
- IL-7Rα+ macrophages may orchestrate cardiac inflammation and potentially regulate lymphocyte responses, influencing myocarditis progression and heart failure development.
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