[The immune stressor effects of T-regulatory cells under infiltrative tuberculosis of lungs].

The article deals with the characteristics of sup-population composition of T-regulator: cells with suppressor activity and production of immunoregulatory cytokines suppressing immune response (IL-10, TGF-beta) in patients with infiltrative tuberculosis of lungs. It is proved that the leading role in formation of immunodepression and tuberculin anergy under infiltrative tuberculosis of lungs is played by T-regulatory, cells with phenotype CD4+CD25+Foxp3+. It is demonstrated that the immunodepression mediated by cytokine production is connected with increasing of both basal and BCG-induced secretion of IL-10 on the background of decrease of level of production of TGF-beta by mononuclear leukocytes in vitro.

The use of ultralow doses of antibodies to C-terminal fragment of angiotensin II AT1 receptor (kardos) in the therapy of arterial hypertension.

Kardos monotherapy allows attaining the target levels of systolic and diastolic blood pressure in patients with high-risk and very-high-risk hypertension. We demonstrated excellent tolerability of the preparation in combination with reliable blood pressure decrease over 24 h, during day and night hours.

Allelic polymorphism of cytokine genes during pulmonary tuberculosis.

Modern immunological and molecular genetic studies showed that tuberculosis is accompanied by an imbalance in the production of immunoregulatory cytokines by mononuclear leukocytes. T allele and homozygous TT genotype of T-330G polymorphism in the IL2 gene, T allele and TT genotype of C-590T polymorphism in the IL4 gene, and CC genotype of A-1188C polymorphism in the IL12B gene are immunogenetic factors that have protective activity against susceptibility to pulmonary tuberculosis. Susceptibility to tuberculous infection is associated with A1A2 genotype of the polymorphic region +3953 A1/A2 in the IL1B gene; G allele and TG and GG genotypes of T-330G polymorphism in the IL2 gene; C allele and CC and CT genotypes of C-590T polymorphism in the IL4 gene; and AC genotype of the polymorphic region A-1188C in the IL12 gene.

[The molecular-genetic aspects of tubercular infection forecasting and immunotherapy].

In article is presented, the analysis of the data of the literature and own researches, concerning molecular-genetic mechanisms of antimycobacterial immunity infringements. The role of the factors defining features of a current and an outcome of a tubercular infection, namely of immunity system condition, feature of infecting microbic Mycobacterium tuberculosis strain biological properties (a genotype, a spectrum of drag sensitivity/resistance), influence of combined antitubercular chemotherapy is disc issed. The opinion is expressed that the given factors are necessary for taking into consideration for working out methodology the personalised preventive maintenance and correction of immunity infringements during pulmonary tuberculosis.

[Role of cytokines in the modulation of lymphocytic subpopulational composition in patients with pulmonary tuberculosis].

The parameters of the lymphocytic CD-population composition and the production of cytokines in the cell cultures of peripheral blood mononuclear cells were studied in patients with infiltrative pulmonary tuberculosis. A marked reduction in the relative and absolute count of CD3+ and CD4+ lymphocytes and an increase in the level of CD8- and CD16-positive cells were established in both drug-sensitive and drug-resistant types of the disease. A significant increase in the production of IL-12 and a reduction in the spontaneous elaboration of interferon-gamma were observed in all the examinees. Addition of lipid and protein myobacterial antigens (Beijing strains) caused a notable decrease in the generation of the study cytokines as compared with the respective parameters in healthy donors and their basal secretion irrespective of the type of a tuberculous process.

[Modulatory effect of isoniazid and rifampicin in vitro on cytokine secretion in pulmonary tuberculosis].

The effects of isoniazid and rifampicin on the peripheral mononuclear production of IL-2, IL-12, IL-10, IFN-gamma, and TGF-beta were evaluated in patients with infiltrative pulmonary tuberculosis. Irrespective of the susceptibility of the causative agent to the essential antituberculous drugs, rifampicin was ascertained to initiate increased IL-2 secretion and to reduce the generation of IL-12, IFN-gamma and TGF-beta. Isoniazid suppressed the mononuclear leukocytic production of IFN-gamma in drug-sensitive pulmonary tuberculosis, and conversely, stimulated it in the drug-resistant type. Rifampicin showed a more significant negative effect on mononuclear cytokine-producing activity. In drug-resistant pulmonary tuberculosis, the imbalance of spontaneous, protein- and drug-induced mononuclear secretion of cytokines was established to be more pronounced than in drug-sensitive tuberculosis.