Intravenous immunoglobulins (IVIG) are currently the most widely used immunobiological drug derived from donor blood. The IVIG preparations contain antibodies, mostly, of IgG class, obtained from plasma pools of 3,000 to 15,000 donors (over 1000 donors per lot, according to international standards and guidelines), being used for treatment of various diseases over four last decades. Initially, IVIG application was
aimed for immune support only in primary immunodeficiency states. However, recent clinical and experimental data show effectiveness of the IVIG in systemic and autoimmune diseases, immune-associated infertility and miscarriage. As well as in translantology, hematology and other fields of medicine. Their efficiency is associated with immunomodulatory effects. There is a growing number of publications bearing on this subject and elucidating possible mechanisms of therapeutic effects of IVIG, which are based on the latest basic and clinical research findings in this area. At the same time, much issues remain unclear and contradictory, and some data are mutually exclusive, thus prompting further studies and trials of IVIG preparations. The aim of this article is to summarize the known basic mechanisms of therapeutic effects, main results of recent research in this area,
and potential clinical applications of IVIG in future.

Our study included measuring the following biological substances: cytokines (IL-1β, IL-6, IFNγ, TNFα, IL-10, TGF-β1, TGF-β2, IL-2, IL-17); soluble receptors to cytokines (IL-2R, IL-6R, TNFαRI and TNFαRII); total serum cholesterol; indicators of intercellular matrix degradation (metalproteinases-9; tissular inhibitor of MMP-9 1 type (TIMP-1); MMP-9/TIMP 1 and MMP-9/TIMP 2 complexes) in 260 patients with clinically manifestations of coronary and lower limb atherosclerosis. Among the patients with atherosclerosis, we have found increased average levels of IL-6, TGF-β2, TNFα RI, TNFαRII, IL-2R, along with decreased IL-2 and IL-10 concentrations, increase of MMP-9/TIMP-2 ratio in blood serum. The following direct correlations were revealed between MMP-9 and IL-1β; between MMP-9/TIMP-1 complex and IL-1β, IL-2, IL-2R, IL-17, IL-10; TIMP-1 with TNFα, IL-2 and IL-2R. At high levels of the general cholesterol, an increased production of TNFα, IL-17, TGF-β1, IL-2, IL-10, MMP-9, TIMP-1 was detected, as well as decreased amounts of TNFα I and TNFαII soluble receptors in blood serum of these patients.
Direct correlations were established between total blood cholesterol levels and IL-2, IFNγ, MMP- 9, TIMP-1, MMP-9/TIMP-2. However blood cholesterol levels showed reverse correlations with TNFαRI, and TNFαRII.
In the course of this study, we have specified a functional imbalance between pro- and anti-inflammatory mechanisms of immune reaction in clinically expressed atherosclerosis. Significant regulatory interactions have been revealed between cytokine levels, total blood cholesterol and markers of intercellular matrix degradation.

We have assumed, that serum production of biological markers that are significantly reflecting a risk degree for atherosclerotic process and acute coronary events may be modified by functional polymorphisms of a functional complex of genes that may be involved into inflammatory process and influence mutual regulation of their production. Therefore, we have assayed a number of appropriate gene polymorphisms and assessed frequency distribution for several promoter genotypes and their combinations, e.c., TNF-A863C; TNF-A308G; TNF-A238G; IL1B C-31T; IL1B-C511T; IL4-C590T; IL6-C174G; IL10A-1082G, IL10-А592C genes, regulatory sites of VEGF-А2578С, VEGF+Т936 gene variants. We have also measured serum levels of TNFα, IL-1β, IL-6, IL-8, IL-1 receptor antagonist (IL-1ra), C-reactive protein, soluble CD40 ligand receptor (sCD40L) in the patients with atherosclerosis. In general, it has been shown that contribution of single cytokine genotypes to the association with level of their production is much lower, than odds ratio of changed protein production associated with a compound genotype.

Aim of study: to examine the features of expression of CD-markers of blood mononuclear leukocytes and their functional activity in the metabolic syndrome. Conducted a cross-sectional (transverse) study of 76 patients with essential hypertension (EH) II stage (BP <180/110 mm Hg.) [10] in conjunction with the metabolic syndrome and 20 people, formed the control group. Along with a complete clinical, laboratory and instrumental examination taken in a specialized cardiological clinic was conducted determination of surface markers of lymphocytes CD4+, CD8+ and monocytes CD36+ and assessment of the level of spontaneous production of reactive oxygen blood mononuclear leukocytes. Found that in patients with the metabolic syndrome compared with the control group the proportion of CD4+ lymphocytes and the level of spontaneous ROS production by mononuclear leukocytes significantly higher. The positive correlated interconnection between these indicators and the number of CD36+ monocytes with the majority of clinical and metabolic markers of MS confirmes their participation in mechanism of immune inflammation and oxidative stress in this pathological process.

Children and teenagers aged 10-17 years old with juvenile arthritis (n=99), with reactive arthritis (n=21), with systemic sclerosis (n=16), with systemic lupus erythematosus (n=14) and conditionally healthy (n=32) are investigated. It’s revealed by the method of flow cytometry that quantity of regulatory T-cells (CD3+CD4+CD25+CD127low/neg) in children with juvenile arthritis, with reactive arthritis and with systemic
sclerosis was lower than in the control group. The amount of Treg in children with systemic lupus erythematosus was the same to the control level. The decrease of Treg number in most of investigated groups indicates that these cells are involved in the pathogenesis of an autoimmune diseases in children. It’s remaining unknown what’s the reason of normal Treg content in patients with systemic lupus erythematosus in contrast with other autoimmune diseases. There were positive correlation between the percentage of Treg and the amount of
damaged joints in children with reactive arthritis and negative correlation between the amount of Treg and SLEDAI in children with systemic lupus erythematosus. The significant correlations between the numbers of CD3+CD25+, CD3+CD4+CD25+ and Treg were revealed, so there isn’t any reasonability of estimation of CD3+ and CD4+cells which are expressed CD25 as separate parameters.

Complicated systemic inflammatory response (SIR) often determines the outcome in patients after cardiac surgery. Systemic endothelial activation plays the most important role in SIR pathogenesis. We have studied the impact of mechanical myocardial injury products, LPS and their combination on human umbilical vein endothelial cells (HUVEC). We have found that HUVEC increase the production of proinflammatory cytokines in response to
cardiomyocyte cytosolic fraction responsible for mechanical injury modeling. 2% cytosolic fraction containing 0.204 ng/mL of Hsp70 was a greater stimulus for endothelial cells to produce IL-6 and IL8 than moderate
endotoxin concentrations.

At present, we are observing eighty-three adult patients with various primary immunodeficiencies (PID) of different origin. The aim of our study was to identify the optimal ways for early detection of such disorders. In this work, we present an analysis of initial clinical manifestations of PID in adults. It was revealed that the type of clinical manifestations is quite unique for individual cases. And the patients exhibit quite diverse clinical findings and course of the disorder, even within a single nosological entity. However, infectious syndrome prevailed among others manifestations. Combinations of complex clinical syndromes were not typical to initial PID pattern. We observed polytopic lesions within each single immunopathological syndrome.

This review concerns studies of compensatory mechanisms in the antioxidant defense, intensification of lipid peroxidation products, assays of local and systemic cytokine profile in COPD patients, thus allowing to determine the molecular phenotypes of systemic inflammatory response. The first of these phenotypes is characterized by certain biomarker combination, i.e., balanced lipid peroxidation and antioxidant defense system, many-fold increase in tissue and systemic concentrations of TFG-β1, high TNFα level. This phenotype is characterized by a moderate immunosuppression, balanced inflammation in respiratory tract. A set of biomarkers typical to the second phenotype may be characterized by activation of free radical lipid oxidation, high levels of of TNFα, bFGF and TGF-β1 secretion, increased sTNFα RI (p55), along with decreased synthesis of a chemoattractant IL-8 cytokine. This phenotype is characterized by an immunosuppressive imbalance causing inflammation in respiratory tract. The third phenotype is associated with the following biomarkers: inactivation of peroxidation processes, high-level secretion of TNFα, bFGF, and sTNFα RI (p55) and decreased TGF-β1 and IL-8 synthesis, thus resulting into imbalanced immunodeficient inflammation in respiratory tract.

We have observed and examined 57 children 1 to 3 years old diagnosed with enlargement of pharyngeal tonsils. A control group was presented by 35 healthy children. Bioluminescence technique was applied for studying NAD(P)-dependent dehydrogenase activity in peripheral blood lymphocytes. Activation of aerobic respiration and increasing activity of pentose phosphate cycle-dependent plastic processes were registered in blood lymphocytes of children with hypertrophic pharyngeal tonsils; along with decreased function of malate-aspartate shunt in energy metabolism of the cells, diminished anaerobic reaction of NADHdependent LDH, lower interaction between Krebs cycle and reactions of amino acid metabolism, and reduced activity of glutathione reductase.

We have studied functional parameters of neutrophilic granulocytes in patients with polypous rhinosinusitis by means of luminol- or lucigeninependent chemiluminescence induced by zymosan and Staphylococcus aureus. Luminol-enhanced chemiluminescence registered the entire pool of reactive oxygen species (ROS), reflecting total activity of myeloperoxidase and NADPH oxidase etc., whereas lucigenindependent chemiluminescence detected production of superoxide radical anion (·О2 -), as well as NADPH oxidase activivity. Usage of the in vitro stimulation tests allows both modeling of disease conditions, and to suggest origins of granulocyte stimulation, their mobilization potential and integration of intracellular processes. We found the increased rate of ROS formation, both in spontaneous and induced chemiluminescent reaction in luminol-dependent process. We have studied neutrophilic granulocyte response to different stimuli and found an increased luminol-dependent ROS formation in polypous rhinosinusitis in response to bacterial induction.