Immunopathological aspects of etiopathogenesis of myocarditis
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https://orcid.org/0000-0001-7924-4048
Abstract
Myocarditis is a group of inflammatory diseases of the heart muscle against the background of the absence of acute or chronic ischemic heart disease, which are diagnosed according to established histological, immunological and immunohistochemical criteria.
Objective. Summarize current information on the immunopathogenesis of myocarditis based on data from open sources of information.
Methods. Publications were selected based on PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases, which covered information on the immunopathogenesis of myocarditis.
Results. Viral infections are the most common cause of myocarditis, along with some bacteria and protozoa. Chronic immune stimulation or autoimmunity in chronic viral myocarditis results from incomplete resolution of the viral infection or response to a previous virus or immune-mediated chronic tissue injury. An active autoimmune response in human myocarditis, both at the cellular and humoral levels, is the immunological basis for the development of this pathology. Myocarditis caused by COVID-19 is a new entity. At the moment, four main manifestations of myocarditis in the context of SARS-CoV-2 have been identified: myocarditis associated with an acute infection of COVID-19, post-acute syndrome of COVID-19 (or prolonged syndrome of COVID-19), multisystem inflammatory syndrome, and myocarditis due to related to vaccination. Autoimmune reactions probably contribute to molecular mimicry – they activate virus-specific T-cells that attack the myocardium. During this phase, high concentrations of cytokines (eg, tumor necrosis factor, interleukins 1a, 1b, 2, and interferon-γ) are produced. These cytokines, together with antibodies against viral and cardiac proteins, further exacerbate cardiac damage and systolic dysfunction due to contractile dysfunction and matrix proteins.
Conclusions. CD4+T-cells are defined as the main driving forces of heart-specific autoimmunity in myocarditis. Dysregulated CD4+ T-cell populations and their associated cytokines are critical for the development and progression of myocarditis and may serve as therapeutic targets and the development of new treatment approaches.
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References
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