IMMUNOLOGICAL FEATURES OF INFLAMMATORY MYOCARDIAL DISEASES DUE TO VIRAL INFECTIONS

Background: Autoantibodies to myocardial antigenic epitopes and corresponding autoreactive T cell clones play an important role in myocardial damage and in pathogenesis of infectious immune myocarditis. T lymphocytes subpopulations/regulatory T cells balance as well as T cell-derived cytokines are crucial in the mechanisms of immune regulation in myocarditis. Aim: To assess quantitative parameters and functional characteristics of basic peripheral blood lymphocytes subpopulations in patients with infectious immune myocarditis and post-myocarditis cardiosclerosis. Material and methods: 35 patients with infectious immune myocarditis and 39 patients with post-myocarditis cardiosclerosis were included. Among infectious immune myocarditis patients, 17 patients had advanced congestive heart failure (CHF) (NYHA III), and 18 patients had mild, moderate or no heart failure (NYHA 0-II). Among cardiosclerosis patients, 18 patients had no CHF, and 21 had only mild symptoms of heart failure (NYHA I). 10 healthy volunteers were enrolled in the control group. Populations and subpopulations of peripheral blood lymphocytes and markers of lymphocytes activation were studied using quadricolor laser flow cytometry (FACSCalibur) and suitable monoclonal antibodies (Becton Dickinson, USA). Results: Inflammatory myocardial diseases are characterized by alterations of innate and adaptive immunity. In our study, patients with infectious immune myocarditis and post-myocarditis cardiosclerosis had significantly reduced numbers of natural killer T cells irrespective of CHF symptoms and disease duration. T cell immunity disturbances were characterized by decreased numbers of CD3+CD4+ cells depending from the disease duration and symptoms severity. Patients with infectious immune myocarditis also had increased numbers of B cells. Immune activation was demonstrated both in infectious immune myocarditis and (less prominent) in post-myocarditis cardiosclerosis. Increased expression of early activation marker CD25 was found during the first 2 weeks from the disease onset in patients with infectious immune myocarditis. In 1 month and during the second month of the disease, increased numbers of T cells and non-T lymphocytes were demonstrated along with late activation manifested by the expression of HLA-DR antigen. Different severity of CHF symptoms was associated with different patterns of activation markers. Increased expression of apoptosis marker CD95 was found in both infectious immune myocarditis and post-myocarditis cardiosclerosis; maximal CD95 values were demonstrated in myocarditis patients in 1 month after the disease onset. Conclusion: Disturbances of anti-infection immunity and self-limitation mechanisms of immune reactions play an important role in the development and progression of inflammatory myocardial diseases.