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EN
Every tumor cell is equipped with an array of biologically active surface molecules, and several these function as receptors for various ligands. They include MHC, or in the case of humans, HLA antigens, cytokine receptors, cell-adhesion molecules, growth factor receptors, Fas/Fas-ligand molecules and others. Their expressions are a subject to alterations, usually to the advantage of tumor growth and spread. Some appear on tumor cells de novo, having no counterparts on the respective normal cells. Detailed knowledge about the expression of tumor-cell receptors and their genotypes, in particular of cancerous ones, may provide information essential for the creation of tools for specific tumor immunotherapy.
EN
Contribution of endothelial cells to normal immune processes (circulation of leukocytes, immune diapedesis, presentation of antigenes) as well as to pathology caused by viral diseases is described.Cytokine secretion and expression of adhesion molecules, particularly during viral infections are described.Permissiveness of endothelial cells to HIV infection is presented.Contrinution of herperviruses (CMV, HSV) to thrombosis and atherosclerosos is also considered.
EN
Adhesion molecules (AMs) are one of the main research areas in biology, cytology and medicine. During last years a great number of AMs was discovered and employed in several mechanisms, including inflammation. Bronchial asthma, allergic rhinitis and conjunctivitis are considered as inflammatory disorders. Based on both in vitro and in vivo studies several mechanisms of selective recruitment eosinophils and basophils through AMs have been developed. Moreover, cytocines, biological peptides and other mediators play role in expression and function of adhesion molecules. Although several aspects of these processes still remains unclear, in vivo data (from animal and human experiments) document the existing of some of these mechanisms. Additional studies, including the use of adhesion molecule antagonists, will clarify the importance of leukocyte adhesion in the pathophysiology of allergic diseases. This review article describes characteristics, properties, regulation of expression and the role of leukocyte- -endothelial adhesion molecules in pathogenesis of allergic diseases.
EN
This paper reviews recent work regarding the molecules that mediate leukocyte-endothelial cell adhesion, describes the underlying principles of laukocyte migration, and discussed a model of the sequence of events that follows a leukocyte to attach to endothelium and migrate into tissue.Pathophysiological importance of the adhesion molecules in the development of different states of inflamation has been also presented.
EN
Aggressive forms of periodontitis lead to rapid bone destruction resulting in extensive losses in children's and young adults' dentition. Adhesion molecule deficiency syndrome and abnormalities in the expression of various adhesion molecules on peripheral blood leukocytes can be observed in prepubertal and aggressive periodontitis (AP) patients. The aim of the study was thus to assess the expression of selected cell adhesion molecules (CAMs; CD11a, CD11b, CD11c, CD54, and CD62L) on monocytes, neutrophils, and lymphocytes of the peripheral blood in patients with AP. The study involved 16 patients with AP and a control group of 13 generally healthy subjects with healthy periodontium. CAM expressions were determined by flow cytometry and presented as mean fluorescence intensity (MIF) and percentage of cells showing expression of the assessed adhesion molecules. Neutrophil CAM expressions in AP patients were comparable with those of the control group. MIF of CD62L on monocytes in AP patients was significantly lower than that of the controls. Lymphocytes showed increased CD11b expression compared with the control group. The percentage of leukocytes showing CAM expression in both groups was similar. Only the percentage of lymphocytes with CD11b in AP patients was significantly higher than in healthy controls. Because of the evident lack of differences between patients and controls and the great amount of individual dispersion of the results, the above CAMs on peripheral blood leukocytes in generally healthy patients with AP do not seem to be characteristic markers of this disease.
EN
The adhesive function of integrins is regulated through cytoplasmic signaling induced by several stimuli, whose process is designated ?inside-out signaling?. A large number of lymphocytes are recruited to the sites of inflammation where they form an essential component of the response to infection, injury, autoimmune disorders, allergy, tumor invasion, atherosclerosis and so on. The recruitment of leukocytes into tissue is regulated by a sequences of interactions between the circulating leukocytes and the endothelial cells. Leukocyte integrins play a pivotal role in leukocyte adhesion to endothelial cells. During the process, the activation of integrins by chemokines, is essential for integrin-mediated adhesion in which a signal transduced to the leukocyte converts the functionally inactive integrin to an active adhesive configuration. The present review documents the relevance of cytoplasmic signaling and cytoskeletal assembly to integrin-mediated adhesion induced by chemokines during inflammatory processes.
EN
Mast cells play a critical role in allergic diseases. When mast cells are activated by cross-linking of their high affinity IgE receptors by the antigen and IgE antibodies, release of chemical mediators is followed by secretion of multiple cytokines. We report that IL-3-dependent mucosal-type mast cells undergo apoptosis when IL-3 is withdrawn. In addition, cross-linking of high affinityIgE receptors prevents apoptosis of mast cells by paractine mechanisms, producing IL-3, IL-4 and granulocyte/macrophage colony-stimulating factor (GM-CSF). However, the secretion of endogenous growth factors are not enough for cell survival, whereas IL-4 induces cell aggregation by expressing adhesion molecules such as leukocyte function-associated antigen 1 (LFA-1), and makes it reactive to endogenous growth factors by contact cell to cell interaction. On the other hand, dexamethazone down-regulates the expression of intracellular adhesion molecule 1 (ICAM-1) and IL-4 in activated mast cells, by which the self-aggregation of mast cells is inhibited and poptosis is induced. Thus, glucocorticoids suppress mast cell survival by inhibiting IL-4 production and expression of adhesion molecules.
EN
Estrogen (E2) was shown to prevent experimental autoimmune encephalomyelitis (EAE) and to produce a novel population of regulatory CD45dimVLA-4+ cells. Although their appearance was dependent upon an elevated hormonal level, E2 was not required for their production, as they also were induced by immunization with Mycobacterium tuberculosis as a component of complete Freund's adjuvant. Materials and Methods: Molecular techniques, including ribonuclease protection assays and quantitative RT-PCR, were used to provide further characterization of CD45dimVLA-4+ cells. Moreover, we determined the developmental requirements of the CD45dimVLA-4+ cells using genetically modified mice and extensive flow cytometry analysis. Results: Characterization of CD45dimVLA-4+ mRNA profile revealed highly elevated levels of CD16, CD44, CCR3, IP-15, and IL-13 transcripts compared with their CD45highVLA-4+ counterparts. Furthermore, we found up-regulation of anti-apoptotic bcl-w and bcl-xl genes and transcripts encoding the TCR and CD8 homodimer. The production of CD45dimVLA-4+ cells was evident in nude mice and in MHC class II- and 2-microglobulin, but not in CD1-deficient mice, suggesting a crucial role for CD1 in their induction.
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