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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-TRI-3156</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-3245</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>ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Тканерезидентные клетки иммунитета в гомеостазе и репарации тканей</article-title><trans-title-group xml:lang="en"><trans-title>Tissue-resident immune cells in homeostasis and tissue repair</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Топтыгина</surname><given-names>А. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Toptygina</surname><given-names>A. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Топтыгина Анна Павловна  – д.м.н., главный научный сотрудник, руководитель лаборатории цитокинов; профессор кафедры иммунологии биологического факультета </p><p>25212, Москва, ул. Адмирала Макарова, 10 </p><p>Тел.: 8 (495) 452-18-30 </p></bio><bio xml:lang="en"><p>Anna P. Toptygina, PhD, MD (Medicine), Head Researcher, Head of the Laboratory of Cytokines;  Professor, Department of Immunology, Faculty of Biology</p><p>10 Admiral Makarov St Moscow 125212</p><p>Phone: +7 (495) 452-18-30 </p></bio><email xlink:type="simple">toptyginaanna@rambler.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФБУН «Московский научно-исследовательский институт эпидемиологии и микробиологии имени Г.Н. Габричевского» Роспотребнадзора; ФГБОУ ВО «Московский государственный университет имени М.В. Ломоносова»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>G.N. Gabrichevsky Research Institute for Epidemiology and Microbiology; Lomonosov Moscow State University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>06</day><month>06</month><year>2025</year></pub-date><volume>27</volume><issue>3</issue><fpage>475</fpage><lpage>484</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Топтыгина А.П., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Топтыгина А.П.</copyright-holder><copyright-holder xml:lang="en">Toptygina A.P.</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/3245">https://www.mimmun.ru/mimmun/article/view/3245</self-uri><abstract><p>Клетки иммунной системы способны свободно заходить в ткани, осуществляя надзорные функции, а затем покидать их, тогда как другие клетки постоянно находятся в нелимфоидных тканях, такие клетки называют тканерезидентными (ТР). В нелимфоидных тканях проживает разнообразное сообщество клеток врожденного и врожденноподобного иммунитета, такие как тканерезидентные макрофаги (ТРМф), лимфоциты врожденного иммунитета (ILC), γδТ-клетки, NKT-, MAIT-клетки, В1- и В-клетки маргинальной зоны. Ранее полагали, что ТР-клетки происходят из гемопоэтических стволовых клеток, однако оказалось, что большинство ТР-клеток происходят из эритромиелоидных предшественников желточного мешка и плодовой печени. ТР-клетки обладают некоторыми признаками «стволовости», а именно, подобно классическим гемопоэтическим стволовым клеткам, они обладают способностью к самоподдержанию. ТР-клетки живут в тканях за счет трофических факторов, вырабатываемых в этих тканях, и сами поддерживают гомеостаз своих ниш. Для ТРМф гомеостатическими факторами являются интерлейкин-34 (IL-34), моноцитарный (M-CSF) и гранулоцито-моноцитарный (GM-CSF) колониестимулирующие факторы, для ILC, γδТ-клеток, NKT- и MAIT-клеток – IL-7 и IL-15, для В1-клеток – IL-5. Представление о том, что существуют всего 4 типа тканей: эпителиальная, соединительная, нервная и мышечная устарело, более подходящей является парадигма минимальных тканевых модулей. При этом каждый модуль состоит из элементов, которые гораздо сильнее взаимодействуют друг с другом, чем с элементами вне модуля. Клетки, объединенные в тканевые модули, оказывают гомеостатическую поддержку другим клеткам, составляющим модуль, при этом являясь нишей для этих клеток, а те оказывают нишевую поддержку для первых. Также ТРклетки оказываются первой линией защиты, поскольку подавляющее большинство патогенов проникают в организм через барьерные ткани. Репопуляция погибших при ответе на инфекцию ТР-клеток осуществляется как в результате пролиферации оставшихся ТР-клеток, так и за счет миграции в ткани клеток костномозгового происхождения. Существуют конкурентные отношения между этими двумя путями репопуляции. При этом ТР-клетки костномозгового происхождения не способны к самоподдержанию и не могут в полном объеме воспроизводить все функции классических ТР-клеток. В процессе регенерации тканей ТР-клетки обеспечивают удаление клеточных отходов и погибших клеток, регулируют воспаление, ремоделируют внеклеточный матрикс и производят факторы роста тканей.</p></abstract><trans-abstract xml:lang="en"><p>Most types of immune cells are able to freely enter tissues, perform surveillance functions, and then leave them, while distinct cells are permanently located in non-lymphoid tissues. Such cells comprise tissue-resident populations (TR). Non-lymphoid tissues are home to a diverse community of innate and innate-like immune cells, such as tissue-resident macrophages (TRMφ), innate lymphocytes (ILC), γδT cells, NKT cells, MAIT cells, B1 cells, and marginal zone B cells. Previously, TR cells were thought to be derived from hematopoietic stem cells, but most TR cells are shown to be derived from erythromyeloid precursors of the yolk sac and fetal liver. TR cells have some features of “stemness”, they have the ability to self-renew, like classical hematopoietic stem cells. TR cells live in tissues due to trophic factors produced within these tissues, thus maintaining homeostasis at their microenvironment. Homeostatic factors for TRMφ are interleukin 34 (IL-34), monocyte and granulocyte-monocyte colony-stimulating factors; for ILC, γδT cells; for NKT and MAIT cells, IL-7 and IL-15; for B1 cells, IL-5. The concept of only 4 types of tissues (epithelial, connective, nervous and muscular) seems to be outdated, a more appropriate paradigm suggests existence of minimal tissue modules. In this case, each module consists of cell elements that interact with each other much more strongly than with elements outside the module. Cell associations within tissue modules provide homeostatic support to other cells that make up the module, being a niche for these cells, thus providing niche support for the former elements. Moreover, TR cells represent the first line of immune defense, since the vast majority of pathogens penetrate the body through barrier tissues. Repopulation of TR cells, that die in response to infection occurs by proliferation of the remaining TR cells, and due to migration of bone marrow-derived cells into the tissues. There are competitive relationships between these two repopulation pathways. At the same time, bone marrowderived TR cells are not capable of self-renewal and cannot fully reproduce all the functions of classical TR cells. TR cells ensure the removal of cellular debris and dead cells, regulate inflammation, remodel the extracellular matrix and produce tissue growth factors.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>тканерезидентные макрофаги</kwd><kwd>ILC</kwd><kwd>NKT-клетки</kwd><kwd>γδТ-клетки</kwd><kwd>В1-клетки</kwd><kwd>тканевой модуль</kwd></kwd-group><kwd-group xml:lang="en"><kwd>tissue-resident macrophages</kwd><kwd>ILC</kwd><kwd>NKT cells</kwd><kwd>γδT cells</kwd><kwd>B1 cells</kwd><kwd>tissue module</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">Топтыгина А.П. Лимфоциты врожденного иммунитета. Неизвестная галактика. //Российский иммунологический журнал, 2014. Т. 8 (17), № 2. С .121-133.</mixed-citation><mixed-citation xml:lang="en">Toptygina A.P. Innate Lymphoid cells. Unknown galaxy. 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