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vol. 48
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issue 5
457-464
EN
Interleukin-15 (IL-15) is a 14-15 kDa polypeptide that belongs to the four alpha-helix bundle family of cytokines and was originally discovered due to its T cell proliferative activity. It utilizes the signal transducing b/g polypeptides of the IL-2 receptor complex thus sharing many biological activities with IL-2, in addition to its high affinity private receptor subunit IL-15Ra. Accumulating evidence indicates that the biological relevance of IL-15 may not solely be confined to T lymphocytes, but to a variety of cell populations within the immune system as well as outside the immune system of the host. The expression of both IL-15 and its high affinity receptor component, IL-15Ra are readily demonstrable in a wide variety of tissues and appear to be augmented in response to environmental/stress stimuli and infectious agents. There is increasing evidence to suggest that IL-15 may play an important role in protective immune responses, allograft rejection and the pathogenesis of autoimmune diseases where mononuclear cell infiltration is a hallmark feature. Herein, the effects of IL-15 on cells associated with host defense, immunity and inflammation are reviewed and support a central role for this cytokine in orchestrating multiple aspects of effector functions in immunity and inflammation.
EN
Monocytes are highly versatile cells, and their functional capabilities include roles as mediators of inflammation and of the immune response. Moreover, monocytes are involved in vascular lesions, due to their interaction with the endothelium and platelets, and they have been imputed to play a relevant role in the pathogenesis of atherosclerosis. The article describes the potential regulatory role of these cells and interaction with platelets in this process.
EN
This report describes the results of applying the computer-assisted image analysis system for the measurement of some cytological parameters of LPS-stimulated and nonstimulated human monocytes. The experiments were carried out by means of the digital cell image analysis of haematoxilyn stained monocytes. Five different parameters describing the morphology of monocytes and their nuclei were selected to quantitate the differences between control and activated cells: area, perimeter, elongation, dispersion, and extension of images of cell projections. The results suggest that all of the analysed parameters can be used to discriminate stimulated from nonstimulated monocytes which permits detailed monitoring of the changes in cell morphology during monocyte activation.
EN
Regulation of monocyte/macrophage function is important to coordinate immune responses. Their contact with invading pathogens activates signaling pathways that provoke pro-inflammatory gene expression and thus causing a locally restricted inflammation. Recently, the peroxisome proliferator activated receptor (PPAR) has been identified to antagonize pro-inflammatory responses in monocytes/macrophages causing an anti-inflammatory and/or desensitized phenotype to predominate. For PPAR general mechanisms in facilitating the transition from a pro- to an anti-inflammatory phenotype have been elucidated. PPAR is a member of the nuclear receptor superfamily and activated upon endogenous as well as exogenous agonist binding. Here we focus on its role in monocyte/macrophage biology in affecting inflammation. Summarizing current information, a model is proposed, giving rise to potential new therapeutic possibilities for the treatment of diseases presumably involving PPAR-dependent regulatory circuits.
EN
CD80 and CD86 seem to play an important role in the allergen induced secretion of IL-5 and IL-13. Up till now, the expression of CD80 (B7.1) and CD86 (B7.2) on monocytes and kinetics of these molecules expression on lipopolysaccharide?stimulated monocytes in nonatopic asthma have not been defined. Using monoclonal antibodies we have compared the expression of CD80 (B7.1) and CD86 (B7.2) on monocytes of healthy persons and nonatopic asthmatic patients. We have also assessed the effect of CD80 and CD86 inactivation on interleukin (IL)-4 and interferon gamma (IFN-gamma production in nonatopic asthmatics and healthy subjects. We found that low expression of CD80 on studied monocytes (1.64+0.65 vs. 3.53+1.43%) and moderate expression of CD86 (41.25+134 vs. 49.46+11.49%) were characteristic for asthma. In nonatopic asthma patients inactivation of CD80 or CD86 blockade significantly reduced IFN-gamma production by T lymphocytes (p<0.02; p<0.03). In both studied groups anti-CD80 antibodies did not diminish T lymphocytes` production of IL-4. However anti-CD86 antibodies significantly (p<0.04) reduced the IL-4 concentration in culture supernatants. Our results confirm that both CD80 and CD86 molecules play on important role in the maintenance and amplification of inflammatory process. It suggests that in the inflammatory process that occurs in the nonatopic bronchial asthma Th1 as well as Th2 lymphocytes are equally important
EN
Mechanical trauma is one of the most important causes of morbidity in the developed world. The response of the immune system to mechanical insult is of paramount importance for the patient's recovery. Shortly after trauma, the indiscriminate saystemic inflammatory response syndrome (SIRS) is mediated by circulating monocytes (Ms) and other innate immunity components. Then acquired immunity, limited to the offending pathogen and the site of injury, gradually preponderates. SIRS is followed by the compensatory anti-inflammatory response syndrome (CARS), where the initial inflammatory response is quenched by anti-inflammatory mediators. This precisely regulated process of immune system activation in response to trauma can be easily deviated, resulting in multi-organ failure (MOF) and increased mortality. Excessive activation of inflammatory Ms in the SIRS phase, premature or exorbitant CARS, a predominance of macrophages (Macs) in the blood stream and peripheral tissues, as well as a depletion of dendritic cells are often seen in trauma patients and contribute to the development of MOF. Here we explore several mechanisms of pathological M? activation in patients with severe mechanical traumatic injury without accompanying sepsis.
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vol. 48
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issue 5
513-520
EN
Infection with Mycobacterium tuberculosis (MTB) is accompanied by an intense local inflammatory response which may be critical to the pathogenesis of tuberculosis. Activation of components of the innate immune response, such as recruitment of polymorphonuclear (PMN) and mononuclear phagocytes and induction of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), by MTB occurs early after MTB infection, however, may persist as the organism establishes itself within granulomas. MTB and its protein and non-protein components are potent in induction of cytokines and chemokines from PMN and monocytes. This review focuses on the interaction of MTB and the host with regard to activation of the innate immune response. It also attempts to identify the potential impact of this early response on the subsequent pathogenesis of MTB, and its role in development and extent of tuberculosis. Insights into the initiation and persistent of the inflammatory response may allow the application of anti-inflammatory agents as adjuncts in the treatment of tuberculosis.
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vol. 40
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issue 2
139-143
EN
The aim of this study was to analyze phenotypes of T cells activated by mitogen (PWM) and antigen (PPD) in the presence of FcR+ or FcR- monocytes. It was found that CD4+ and CD8+ lymphocytes are preferentially acitvated in the presence of different subpopulations. Expression of HLA-DR and CD25 on CD4+ lymphocytes was greater in cultures activated in the presence of FcR-. CD8+ lymphocytes were more efficiently activated (exprression of HLA-DR) when FcR+ monocytes were added to culture. In the presence of FcR+ monocytes an increased expression of CD45RA antigen on CD4+ cells was also observed. These data support our previous functional studies which showed that "suppressor" T cells of CD8+ phenotype are activated in the presence of FcR+ monocytes.
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