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In most solid tumors, tumour associated macrophages (TAM) are known to be unable to demonstrate cytotoxic and antitumor activity. As an explanation of this phenomenon, production of immunosuppressive cytokines by tumor cells are usually provided. Despite this, attempts remain to be made to change the macrophage phenotype from M2, characteristic of TAM, to M1, which has antitumor activity. Most of these attempts remain unsuccessful, which indicates the possible presence of macrophages that have lost the ability to respond to bacterial components as a result of tolerance induction. Recently, more and more attention has been paid to the study of the microbiological component of the tumor stroma. Studies have shown that the vast majority of solid tumors contain complex bacterial populations that differ from those of normal tissues. Certain correlations were found between the number and composition of the tumor microbiota and the course of the disease or response to treatment. One of the functions of macrophages is the response to a bacterial infection, which also implies a corresponding response to bacteria inside the tumor. Depending on the amount of the bacterial stimulus, macrophages can both activate and stimulate the inflammatory response, in the case of a large amount of pathogen, and go into a state of tolerance, that is, not only do not respond adequately to the primary stimulation, but also lose the ability to respond to repeated stimulation by the pathogen . The presence of this type of macrophage in tumors explains the inability of TAM to activate their cytotoxic function, even when stimulated by bacterial components as a drug. The properties of these cells must be taken into account when developing new methods for the immunotherapy of tumors. Earlier, we obtained data on the quantitative and qualitative composition of the microbiota of lung tumors. The data obtained clearly indicate the presence of bacteria in the tumor that can cause the formation of tolerant macrophages.
грант РФФИ |
# | Сроки | Название |
1 | 9 января 2020 г.-31 декабря 2022 г. | Механизм развития толерантности макрофагов в опухолях легкого |
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