Related Experiment Video
Updated: Aug 20, 2026

Flow Cytometry-Based Quantification and Analysis of Myocardial B-Cells
Published on: August 17, 2022
Myocarditis, microbes and autoimmunity
J Lindsay Whitton1, Ralph Feuer
1Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037, USA. lwhitton@scripps.edu
Abstract:
Acute and chronic myocarditis can be caused by a number of infectious agents, including viruses, bacteria and protozoa. These diseases are refractory to treatment, and the development of rational therapies will require a detailed understanding of the mechanisms that underlie the pathological inflammatory responses. Here, we review three infectious myocarditides that, despite the dissimilarity of the microorganisms, share several common features: (i) the microbes replicate in the heart; but (ii) are difficult to isolate, in infectious form, during chronic disease; (iii) autoreactive antibodies and T cells specific for cardiac antigens have been identified in infected animals; and (iv) these autoreactive responses have been proposed as the main effectors of cell death, and myocardial damage. We critically evaluate the data, and we suggest that the findings can be reconciled without invoking autoimmunity as an effector mechanism. Alternative hypotheses to explain the tissue destruction are proposed.
Insights
Infectious myocarditis, often difficult to treat, involves microbes in the heart. This review questions autoimmunity as the primary cause of heart damage, proposing alternative explanations for tissue destruction.
Area of Science:
- Cardiology
- Immunology
- Infectious Diseases
Background:
- Myocarditis, encompassing acute and chronic forms, stems from diverse infectious agents like viruses, bacteria, and protozoa.
- Current treatments for myocarditis are often ineffective, highlighting the need for deeper mechanistic understanding to develop targeted therapies.
- Understanding the pathological inflammatory responses is crucial for advancing myocarditis treatment strategies.
Purpose of the Study:
- To review three distinct infectious myocarditides with shared characteristics.
- To critically evaluate the proposed role of autoimmunity in myocarditis pathogenesis.
- To propose alternative mechanisms for myocardial damage in infectious myocarditis.
Main Methods:
- Literature review of infectious myocarditides.
- Analysis of common features across different infectious myocarditides.
- Critical evaluation of existing data on autoimmune responses in myocarditis.
Main Results:
- Identified common features in three infectious myocarditides: cardiac microbial replication, difficulty in isolating infectious agents during chronic disease, and presence of autoreactive antibodies and T cells.
- Challenged the prevailing hypothesis that autoreactive responses are the main effectors of cell death and myocardial damage.
- Highlighted the need to reconcile findings without solely relying on autoimmunity as an effector mechanism.
Conclusions:
- The proposed role of autoimmunity in infectious myocarditis requires re-evaluation.
- Alternative hypotheses for myocardial tissue destruction in infectious myocarditis are presented.
- Further research is needed to elucidate the precise mechanisms underlying infectious myocarditis and guide therapeutic development.
Related Concept Videos
Myocarditis I: Introduction
Myocarditis II: Clinical Features and Diagnostic Tests
Myocarditis III: Medical Management
Autoimmune Disorders
Concept and Mechanism of Autoimmune Diseases
The immune system...
Endocarditis I: Introduction
Myocarditis IV: Nursing Management
