Introduction. Traumatic brain injury (TBI) is one of the common diseases of the person, which is accompanied by high mortality and disability of the victims. In the pathogenesis of TBI there are at least 2 periods that are associated with both primary nerve cell injury by the traumatic factor and secondary inflammatory-destructive changes that develop over a long period after the injury. An important role in the development of the second period of TBI is played by the body’s immune system, which can complicate the course of TBI and act differently depending on the severity of the injury. The goal of the work. The work investigated the state of proliferative and cytotoxic ability of splenocytes in light TBI in rats, which was caused by a drop in weight of 50 g from a height of 120 cm per animal. Materials and results. Studies have shown that within 24 hours after injury, there is an increase in the proliferative activity of splenocytes in the test for proliferation with mitogens, especially with KonA mitogen. While the cytotoxic activity of splenocytes is significantly inhibited at this time and the number of hyperdiploid cells in the spleen is reduced. At a later date after the injury, for 5 days, there is a significant recovery of immunological parameters, indicating that from the first hours after a mild TBI, the immune system changes in different directions, mainly towards the activation of proliferation, which may complicate the course the traumatic period. Conclusions. In experimental mild TBI, rats have differentiated changes in the activity of immune cells, which indicate the activation of the immune system in the early stages after injury.
This review presents data on changes in the activity of cells of innate and acquired immunity, namely leukocytes, neutrophils, platelets and lymphocytes in various malignant human tumors, including brain tumors. It was shown that against the background of immunosuppression of specific immunity, especially antitumor reactions, which are caused by factors such as prostaglandin E2, TGF-β, indolamine-2,3-dioxigenase (IDO) and interleukin (IL) -10, which leads to a decrease the sensitivity of T cells to proinflammatory signals and the ineffectiveness of the presentation of tumor antigens to immune cells, activation and polarization of innate immunity cells, namely neutrophils, macrophages and platelets, occurs. Macrophages are important immune cells of the microenvironment in a tumor site that change their phenotype from M1 cells with antitumor activity to M2, which enhance tumor growth. The release of metalloprotheasis from platelet α -granules destroys the components of the extracellular matrix, increases the ability of cancer cells to pass through the endothelial barrier, penetrate the parenchyma and create metastatic tissue damage. Previously, neutrophils were mainly considered as cells of the body’s first line of defense, mainly with antimicrobial functions, but now they are regarded as cells with tumor-stimulating, “protumorogenic” activity, since in many types of cancer an increased level of neutron is determined with a reduced content of lymphocytes in the peripheral blood and this is associated with a poor prognosis of the disease. The review analyzes the hypothesis that there are three subpopulations of neutrophils in cancer: normal high density neutrophils, immature low density neutrophils (G-MDSC) and large mature low density neutrophils. These types of cells have different functions, for example, neutrophils with high density are antitumor, and with low density - cells that can stimulate tumor growth. ]. Neutrophils realize their activity through molecules such as neutrophilic elastase (NE), cathepsin, arginase 1 (ARG1), matrix metalloproteinase-9 (MMP-9). Multidirectional changes in the parts of the immune system depend on the histogenesis and degree of malignancy of the tumors and indicate differentiated use immunotropic drugs in cancer patients, some should suppress the activity of innate immunity cells, others stimulate the acquired immune response.
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