[Cytokines as a diagnostic and therapeutic tool in patients with myocarditis]

One of the leading causes of autoimmune myocardial lesion in patients with myocarditis is disbalance between pro-inflammatory and anti-inflammatory cytokines, leading to the loss of functional tolerance to certain myocardial autoantibodies, and activation of autoreactive T-lymphocytes, which are able of myocardial cytotoxicity. The authors have conducted studies, which have shown that malignant myocarditis is characterized by abrupt increase of TNF-alfa and IFN-alfa basal serum levels, while at the same stage of the disease in patients with benign myocarditis only moderate increase of TNF-alfa level is observed, and IFN-alfa concentration is within normal limits. Abrupt increase of the cytotoxic activity of lymphocytes, activated by IL-2 (LAK-cells), is a feature of malignant myocarditis. In this category of patients the studies have found pronounced disbalance between cytokine serum levels, with abruptly increased levels of both cytokines which activate cytotoxic reactions (TNF-alfa, IFN-alfa, IL-1 alfa, IL-1 beta, IL-12), and cytokines which stimulate humoral immunity (IL-4 and IL-6), and increase of antimyocardial autoantibody concentration. Further research into the role of cytokines in myocarditis pathogenesis would allow grounded cytokinotherapy and application of immunomodulators, activating cytokine production.