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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">mimmun</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинская иммунология</journal-title><trans-title-group xml:lang="en"><trans-title>Medical Immunology (Russia)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1563-0625</issn><issn pub-type="epub">2313-741X</issn><publisher><publisher-name>SPb RAACI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15789/1563-0625-ICO-2011</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-2011</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>КРАТКИЕ СООБЩЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SHORT COMMUNICATIONS</subject></subj-group></article-categories><title-group><article-title>Иммунологический контекст легкой травмы головного мозга</article-title><trans-title-group xml:lang="en"><trans-title>Immunological context of brain injury</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8701-7213</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Плехова</surname><given-names>Н. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Plekhova</surname><given-names>N. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Плехова Наталья Геннадьевна – д.б.н., заведующая центральной научно-исследовательской лабораторией</p><p>690002, г. Владивосток, пр. Острякова, 2</p></bio><bio xml:lang="en"><p>Plekhova Natalya G., PhD, MD (Biology), Head, Central Research Laboratory; Leading Research Associate, Laboratory for Composite Coatings of Biomedical Applications</p><p>690002, Vladivostok, Ostryakov ave., 2</p><p> </p></bio><email xlink:type="simple">pl_nat@hotmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Радьков</surname><given-names>И. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Radkov</surname><given-names>I. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант центральной научно-исследовательской лаборатории</p><p>г. Владивосток</p></bio><bio xml:lang="en"><p>Postgraduate Student, Central Research Laboratory</p><p>Vladivostok</p></bio><email xlink:type="simple">radiarest@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6022-6130</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зиновьев</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Zinoviev</surname><given-names>S. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., старший научный сотрудник центральной научно-исследовательской лаборатории</p><p>г. Владивосток</p></bio><bio xml:lang="en"><p>PhD (Medicine), Senior Research Associate, Central Research Laboratory</p><p>Vladivostok</p></bio><email xlink:type="simple">sinowev@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9645-3471</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шуматов</surname><given-names>В. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Shumatov</surname><given-names>V. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, ректор</p><p>г. Владивосток</p></bio><bio xml:lang="en"><p>MD, PhD (Medicine), Professor, Rector</p><p>Vladivostok</p></bio><email xlink:type="simple">mail@tgmu.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Тихоокеанский государственный медицинский университет» Министерства здравоохранения РФ; ФГБУН «Институт химии Дальневосточного отделения Российской академии наук»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pacific State Medical University; Institute of Chemistry, Far Eastern Branch, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБОУ ВО «Тихоокеанский государственный медицинский университет» Министерства здравоохранения РФ</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pacific State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>26</day><month>02</month><year>2021</year></pub-date><volume>23</volume><issue>1</issue><fpage>163</fpage><lpage>168</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Плехова Н.Г., Радьков И.В., Зиновьев С.В., Шуматов В.Б., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Плехова Н.Г., Радьков И.В., Зиновьев С.В., Шуматов В.Б.</copyright-holder><copyright-holder xml:lang="en">Plekhova N.G., Radkov I.V., Zinoviev S.V., Shumatov V.B.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.mimmun.ru/mimmun/article/view/2011">https://www.mimmun.ru/mimmun/article/view/2011</self-uri><abstract><p>Параметры нескольких популяций иммунных клеток (Т-клетки и макрофагальные субпопуляции) изучали в периферической крови и головном мозге на клинически релевантной модели легкой травмы головного мозга (ТГМ) у крыс. Популяция резидентных клеток врожденного иммунитета, состоящая из микроглии и астроцитов при локальном повреждении тканей вовлекается в реализацию воспалительного ответа. В ситуации с травмой показано также, что лейкоциты крови могут преодолевать гемато-энцефалический барьер и проникать в паренхиму головного мозга. Использовали методы проточной цитометрии и иммунофлуоресценции. Было отмечено повышение числа моноцитов и нейтрофилов в срок до 1 сут. после легкой ТГМ, с последующим снижением к концу сроков наблюдения. Было установлено, что число CD45+ клеток и CD3+T-клеток снижалось через 1 день после ТГМ и постепенно росло до 14 сут., а процент CD4+T-клеток постоянно снижался с 7 до 14 сут., тогда как доля CD8+T-клеток повышалась с 7 до 14 сут. наблюдения. При легкой ТГМ у животных наблюдалось значительное снижение (в 3-10 раз) числа микрососудов с позитивной реакцией на SMI 71 на 8-й и 14-й день после травмы головы. Интенсивная окраска микрососудов на SMI 71 иногда сочеталась с расширением области позитивной реакции. Тонкие позитивные отложения продуктов наблюдадись в головном мозге здоровых животных вокруг стенок микрососудов. В поврежденной ткани головного мозга выявлялись макрофаги, позитивные по CD45high/CD11b+ популяции M1 на второй день после ТГМ и отмечались в значительном количестве на 8-14-й день. В мозолистом теле и ипсилатеральном участке стриатума содержание клеток, экспрессирующих CD16/11b+, достигало максимума через 8 сут. после травмы, что коррелировало со снижением позитивного ответа на наличие эндотелиального антигена SMI 71. Таким образом, в остром периоде после легкой ТГМ в головном мозге определяется наличие иммунопатологических процессов, что может впоследствии вести к дизрегуляции нейроиммунных связей.</p></abstract><trans-abstract xml:lang="en"><p>The parameters of several populations of immune cells (T cell populations, macrophage subpopulations) in peripheral blood and brain were studied in a clinically significant model of mild traumatic brain injury among rats. The population of resident cells of innate immunity of microglia and brain astrocytes with local tissue damage is involved in the implementation of the inflammatory response, it is also shown that in case of trauma, blood leukocytes can overcome the blood-brain barrier and penetrate the brain parenchyma. The methods of flow cytometry and immunofluorescence were used. An increase in the number of monocytes and neutrophils up to 1 day, after a mild traumatic brain injury (TBI) with a subsequent decrease to the end of the observation period was noticed. It was determined, that the number of CD45+ cells, CD3+T cells decreased at 1 days post-injury (dpi), and rose slightly by 14 dpi, the percentage of CD4+T cells continuously declined from 7 to 14 dpi, while the percentage of CD8+T cells increased from 7 to 14 dpi. With mild traumatic brain injury in animals, a significant (3-10 times) decrease in the number of microvessels with a positive reaction to the presence of SMI 71 on the 8th and 14th day after head injury was observed. Intensive staining of SMI 71 microvessels was sometimes observed with an increase in the area of a positive reaction. Thin positive deposits of the reaction product are observed in the brain of healthy animals around the wall of the microvessel. In the damaged brain, CD45high/CD11b+ positive macrophages of the M1 subpopulation appeared in the brain tissue on the 2nd day after TBI and a significant amount was observed on the 8-14th day. In the corpus callosum and ipsilateral region of the striatum, the content of cells expressing CD16/11b+ reached a maximum 8 days after TBI, which correlated with a decrease in the positive response to the presence of endothelial antigen SMI 71. Thus, in the acute period of mild TBI, the presence of neuroimmunopathological processes is determined in the brain, which can subsequently result to the dysregulation of neuroimmune connections.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>нейроиммунология</kwd><kwd>микроглия</kwd><kwd>врожденный и адаптивный иммунитет</kwd><kwd>легкая травма головного мозга</kwd></kwd-group><kwd-group xml:lang="en"><kwd>neuroimmunology</kwd><kwd>microglia</kwd><kwd>innate and adaptive immunity</kwd><kwd>mild traumatic brain injury</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Bai R., Gao H., Han Z., Huang S., Ge X., Chen F., Lei P. Flow cytometric characterization of T cell subsets and microglia after repetitive mild traumatic brain injury in rats. Neurochem. 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