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Purpose of the study. To evaluate the number of cells with the CD45+/- phenotype expressing Toll-like receptors (TLRs) in tissues of the tumor, peritumoral area and resection line tissues in colon cancer (CC) with various tumor locations.Materials and methods. The study included 50 patients with CC. All patients underwent surgery as the primary treatment, and tissue material was collected from the patients. Expression of TLRs (2, 3, 4, 8, 9) on CD45+, CD45- cell populations was determined by flow cytometry in cell suspensions obtained from tissues of the tumor, peritumoral area (1–3 cm from the tumor) and resection line tissues (~10 cm from the tumor) with further calculation of the percentage of cells with the corresponding phenotype from the total number of cells.Results. An analysis of left-sided colon tumors showed lower percentage of CD45- cells expressing TLR4, 8, compared to rightsided tumors, by 38 % and 25 %. A comparative analysis of the number of CD45+ cells expressing TLR 2, 4 showed their decrease by 81 % and 87 %, respectively, compared with right-sided tumors. An assessment of the data in the perifocal zone of left-sided colon tumors, compared with right-sided ones, demonstrated a decrease in the percentage of cells with the CD45- phenotype that express TLR4, by 61 %. Resection line tissues in left-sided tumors, compared with right-sided ones, showed a statistically significant increase in the percentage of CD45- cells that express TLR 2, 4 by 205 % and 55 %, respectively. The number of CD45+ cells expressing TLR 4 decreased by 87 %. An assessment of the number of cells expressing TLRs 3 and 9 in the tumor, peritumoral area and resection line tissues did not reveal significant differences.Conclusions. Lower number of cells with CD45+ and CD45- phenotypes express TLRs 2, 4, 8 in left-sided colon tumors and their peritumoral tissues, compared to right-sided cancer.

Aim. The study of the mechanisms of atopic disease formation and a model of immunopathogenesis of the atopic diseases.Methods. Determination of surface lymphocytes receptors in peripheral blood of atopic bronchial asthma and atopic dermatitis patients with the help of monoclonal antibodies using the indirect immunofluorescence method. Expression of genes encoding TLR2, TLR4 and TLR9 receptors of airborne epithelial cells by real-time polymerase chain reaction, as well as determination of cytokine TSLP, IL-33, IL-4 and TGFβ (eBioscience) in airway flushes in atopic asthma patients and healthy people.Results. During the exacerbation of atopic diseases in peripheral blood lymphocytes, an intensive activation process develops with impaired lymphocytes activating apoptosis aimed at the formation of plasma cells capable of developing intensive IgE synthesis. To search for signals that could explain the mechanism of rearrangement of the B-cell part of the immune system during atopy, the epithelium cells of the airways were examined in a group of patients with atopic asthma and found an increase in gene expression coding for TLR2, TLR4, TLR9 in 6, 3 and 2.5 times respectively. Along with increased expression of TLRs genes in patients with bronchial asthma, an increased content of TSLP and IL-33 cytokines secreted by epithelial cells of the airways was detected. These cytokines have an immunoregulatory action - their nearby antigen presenting functions format the Th2 type of immune response, promote the production of cytokines (IL-4, IL-9, IL-13) and cause the development of an allergic type of inflammation.Conclusion. We suppose that the main link in pathogenesis is a disruption of the interaction of TLRs with the corresponding ligands caused by spontaneous dimerization of TLRs under the malonic dialdehyde influence. The intake of slowly metabolized dimers of TLRs into epithelial cells is a signal for genome activation, which leads to the synthesis of allergic cytokines IL-33 and TSLP. Thus, the main immunopathogenesis pathway of atopic diseases is the pathological functional interaction between epithelial cells and peripheral blood B-lymphocytes.

Background. At present many authors associate pathogenesis with the defect in genes polymorphism of key cytokines and the genes defect of Toll-like receptors (TLRs) of congenital immune system. The objective of this study was to analyze key cytokines indicators IL-4, IL-6, IL-10, IL-18, FNO-α, TGF-β, IFN-γ, associations of genes polymorphism IL-2, IL-4, IL-17A and TLR2, TLR4, TLR3, TLR9 in pyoderma patients. Materials and methods. Over the study period 98 patients with pyoderma (chronic recurrent furuncles, sycosis) were examined 45 healthy persons (control group) were examined as well. The age was from 18 to 65. The indicators IL-10, IL- 18, TGF-β, IL-4 in supernatants of stimulated cells had been study was determined by enzyme immunoassay. The variants of genes IL-2, IL-4, IL-17A и TLR2, TLR4, TLR3, TLR9 were typified by polymerase chain reaction with the detection of amplification products in the «real time» mode. Results. The increase of indicators IL-10, IL-18, TGF-β, IL-4 in blood serum and the decrease of indicators of induced IFN- γ were identifiti in pyoderma patients comparing to control group. This fact proves that pyoderma patients are in immunodeficiency condition by humoral type with predominated Th2 immune response. The increase of genotype prevalency A/A of polymorphism (G-197A) of gene IL- 17A in pyoderma patients can be related to the impact deficiency of Th17 on neutrophils. It can result in predisposition to skin diseases of infectious genesis. The decrease of genotype A/A and increase of genotype A/G polymorphism (A-753G) of gene TLR-2 in pyoderma patients can result in lack of response into lipopolysaccharids and selective disfunction of protecting reactions against gram-positive bacteria. Conclusions. Predominance of Th2 type of immune response and revealed defects of polymorphism (G-197A) of IL-17A gene and polymorphism) (A-753G of TLR2 gene in patients with pyoderma will contribute to understanding of immunogenetic bases of disease formation for use in clinical practice.

Treatment of malignant tumors is among challenging issues of clinical medicine. Dissemination and matestasis of tumor cells plays a major role in oncology, being immediately dependent on chemotaxis of tumor cells. Hence, the aim of our study is to evaluate migration of tumor cells, in terms of ligand-mediated chemotaxis of a human U 937 lymphoma cell line. Synthetic TLR ligands (DNA_lig, RNA_lig) were used as chemoattractants. Assessment of time-dependent TLR expression by the migrating cells (including TLR2, TLR3, TLR7, TLR9) was carried out by means of real-time PCR, using Boyden’s chamber system for the migration assays. We have revealed an increased cell migration towards DNA_ lig and TNFα gradient. Expression of TLR2, TLR7 and TLR9 was found to be increased under the influence of TNFα (respectively 1.5-, 4- and 19-fold). Under the influence of DNA_lig, TLR9 expression was 105-fold increased, whereas TLR3 expression was 2-fold higher, along with decrease of TLR2 expression. Expression of TLR 3 was shown to be 3-times higher under the influence of RNA_lig. The effects observed could be potentially applied for suppression of tumor cell chemotaxis by means of these ligands and by influencing different pathways ofchemotaxis regulation.

Abstract. The mechanisms of the immune system responding to an infection depend on a complex interrelation between the elements of innate and adaptive immunity. The current understanding of how signaling from innate immunity receptors shapes the adaptive immune response against pathogens and how it looks like the adaptive control of innate immunity are discussed in the article. One of the main problem needed to be highlighted is if adaptive immune cells suppress or activate innate immunity? Several studies yield new light to the question how the adaptive immunity can compensate, suppress and activate innate immunity. The role of inflammatory signals of dendritic cells activation in induction and modulation of adaptive immunity is described. Innate immunity receptors instruct the adaptive immune system on when and how to best respond to a concrete infection.