The goal of our research was comparative study of the most important parameters of subset cytoarchitectonics in the patients with the different courses of myocarditis and evaluation of their pathoge$ netic and clinical value in the practice of the physician. We have investigated 99 patients with myocarditis and 40 healthy donors. In patients with malignant course of

Abstract. The goal of our research was comparative study of the most important parameters of subset cytoarchitectonics in the patients with the different courses of myocarditis and evaluation of their pathogenetic and clinical value in the practice of the physician. We have investigated 99 patients with myocarditis and 40 healthy donors. In patients with malignant course of disease we revealed increased activation index of T/B-cells; increased expression of the activation markers on the both lines of differentiation; disproportion in the immunoregulatory subsets with increased role of dendric cells; decreased intensity of the autoreactive T-cells apoptosis. in the patient with the In patients with nonmalignant course of disease expressed signs of immunopathology were not found. Thus, study of activation markers on the cells of the peripheral blood is more informative and noninvasive method of diagnostics of myocarditis.

Abstract. In glioblastoma (GB), it is necessary to take into consideration GB-associated secondary immunodeficiency (SID), so-called syndrome of tumor-associated SID (STASID). Cell subsets having effector and regulatory functions, play an important role in developing STASID, and their proportions in patients with different forms of GB can be of pathogenetic importance and have clinical value for treatment and rehabilitation scheduling as well. The most pathogenically and clinically important features of cell subsets profile of peripheral blood were analyzed in patients with different clinical and morphological types of GB. The patients were divided into three groups, i.e., groups I and II were formed by patients with STASID (marked and slightly marked SID, accordingly); group III – patients with SIDTAS (tumor-associated autoimmune syndrome, associated with SID). Marked suppression of cell immunity is typical of group I - imbalance in T-lymphocytes, in a number of specific subsets, and in subsets clusters, as well as disproportions in the immunoregulatory indexes. In group II, the subset profiles of blood were slightly different from the norm. In patients with SIDTAS, activation of cell immunity was evident, forming SID with signs of autoimmune syndrome, affecting effector and regulatory chains of immunity, and influencing the severity and forecast of the disease. Specific features of the immune status in patients with GB identified can be resulted from different clinicalmorphological types of the tumor; the latter are to be considered in differential diagnostics of clinical course of GB and in scheduling of clinical-immunological efficient anti-tumor pharmacotherapy in pre- and postoperative periods.

AIM:To study possible immunogenetic HLA markers of chronic viral hepatitides.MATERIAL AND METHODS:Using the reaction of complement-dependent cytotoxicity by Terasaki, we analysed distribution of leukocytic HLA antigens (loci A, B and C) in 179 patients with chronic viral hepatitides B, C and D in Russians and Kazakhs living in the Astrakhan Region.RESULTS:In the Russian population we discovered a significant positive association of CVHB with HLA-B18, HLA-B35, HLA-B40, HLA-Cw3 antigens, and negative one--with HLA-A2. In Kazakhs with CVHB there was a positive association with HLA-A3, HLA-B18 and negative one--with HLA-A11. Alleles HLA-A10, HLA-B35, HLA-B40 and HLA-Cw3 mark CVHC in Russians. HLA-Cw4 specificity acts as protector in development of chronic HCV-infection. A correlation was found between carriage of some specificities and haplotypes of HLA and activity of chronic HBV and HCV infection. A high risk of chronic delta infection in Russians is associated with HLA-B8 and HLA-B35, in Kazakhs--with HLA-B35 and HLA-D40. There are significant associations between CVHB, CVHC, chronic delta infection and some HLA haplotypes.CONCLUSION:A universal role of HLA-B35 specificity in development of CVH irrespective of hepatotropic virus and patients' nationality is shown.

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.

AIM:To elucidate the role of tumor necrosis factor alpha (TNF alpha) and interferon alpha (INF alpha) in pathogenesis of infectious-immune myocarditis (M) and myocarditic cardiosclerosis (MCS).MATERIAL AND METHODS:Patients with infectious-immune myocarditis (n=27) and myocarditic cardiosclerosis with symptoms of heart failure (n=19). Blood levels of TNF alpha and INF alpha were measured by immune enzyme analysis.RESULTS:Mean levels of INF alpha and TNF alpha in patients with M (75+/-47 and 304+/-102 rg/ml respectively) were significantly higher than in patients with MCS and healthy donors (31+/-14 and 83+/-39; 38+/-18 95+/-58 rg/ml, respectively, p<0.05). Levels of INF alpha and TNF alpha significantly differed between patients with benign and malignant course of M (99+/-46 and 354+/-100; 39+/-10 227+/-42 rg/ml, p<0.05). Phytohemagglutinine induced TNF alpha production by leucocytes in patients with malignant M (1432+/-515 rg/ml) was higher (p<0.05) while in patients with benign M (131+/-54 rg/ml) lower (p<0.01) than in healthy donors (255+/-98 rg/ml). Patients with malignant compared with those with benign course of myocarditis had lower ejection fraction (25.9+/-12.1 and 42.5+/-11,2%, respectively, p<0.003) and higher inhospital mortality (16.6 and 0%, respectively).CONCLUSION:It is most probable that factors of regulation of INF alpha and TNF alpha production occupy an import place among mechanisms of malignant transformation of myocarditis.