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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">10.15789/1563-0625-2018-4-477-484</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-1557</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>ИНТЕРЛЕЙКИН-33 И ФИБРОЗ: СОВРЕМЕННЫЙ ВЗГЛЯД НА ПАТОГЕНЕЗ</article-title><trans-title-group xml:lang="en"><trans-title>INTERLEUKIN 33 AND FIBROSIS: PATHOGENESIS UPDATED</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>Учасова</surname><given-names>Е. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Uchasova</surname><given-names>E. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., старший научный сотрудник лаборатории исследований гомеостаза отдела диагностики сердечно-сосудистых заболеваний,</p><p>650002, г. Кемерово, Сосновый бульвар, 6</p></bio><bio xml:lang="en"><p>PhD (Medicine), Senior Research Associate, Laboratory Research Homeostasis,</p><p>650002, Kemerovo, Sosnovy bvld, 6</p></bio><email xlink:type="simple">evg.uchasova@yandex.ru</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>Груздева</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Gruzdeva</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., заведующая лабораторией исследований гомеостаза отдела диагностики сердечно-сосудистых заболеваний;</p><p>доцент кафедры патологической физиологии, медицинской и клинической биохимии,</p><p>г. Кемерово</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Head, Laboratory Research Homeostasis;</p><p>Associate Professor, Department of Pathological Physiology, Medical and Clinical Biochemistry, </p><p>Kemerovo</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Дылева</surname><given-names>Ю. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Dileva</surname><given-names>Yu. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., научный сотрудник лаборатории исследований гомеостаза отдела диагностики сердечно-сосудистых заболеваний,</p><p>г. Кемерово</p></bio><bio xml:lang="en"><p>PhD (Medicine), Research Associate, Laboratory Research Homeostasis, </p><p>Kemerovo</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каретникова</surname><given-names>В. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Karetnikova</surname><given-names>V. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, заведующая лабораторией патофизиологии мультифокального атеросклероза отдела мультифокального атеросклероза;</p><p>профессор кафедры кардиологии и сердечно-сосудистой хирургии,</p><p>г. Кемерово</p></bio><bio xml:lang="en"><p>PhD, MD (Medicine), Professor, Head, Pathophysiology Laboratory of Multifocal Atherosclerosis;</p><p>Professor, Department of Cardiology and Cardiovascular Surgery, </p><p>Kemerovo</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний»<country>Россия</country></aff><aff xml:lang="en">Research Institute for Complex Issues of Cardiovascular Diseases<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний»;&#13;
ФГБОУ ВО «Кемеровский государственный медицинский университет» Министерства здравоохранения РФ<country>Россия</country></aff><aff xml:lang="en">Research Institute for Complex Issues of Cardiovascular Diseases;&#13;
Kemerovo State Medical University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>25</day><month>06</month><year>2018</year></pub-date><volume>20</volume><issue>4</issue><fpage>477</fpage><lpage>484</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Учасова Е.Г., Груздева О.В., Дылева Ю.А., Каретникова В.Н., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Учасова Е.Г., Груздева О.В., Дылева Ю.А., Каретникова В.Н.</copyright-holder><copyright-holder xml:lang="en">Uchasova E.G., Gruzdeva O.V., Dileva Y.A., Karetnikova V.N.</copyright-holder><license 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/1557">https://www.mimmun.ru/mimmun/article/view/1557</self-uri><abstract><p>Интерлейкин-33 (IL-33) член семейства IL-1, который широко экспрессируется во всех типах клеток. IL-33 был идентифицирован как функциональный лиганд для рецепторного комплекса плазматической мембраны, который представляет собой гетеродимер, состоящий из связанного с мембраной рецептора ST2 (стимулирующий фактор роста). IL-33 участвует в развитии иммунного ответа с преимущественным высвобождением провоспалительных цитокинов Т-хелперов 2 типа. IL-33 широко экспрессируется в различных структурных клетках, таких как эпителиальные, эндотелиальные и клетки гладкой мускулатуры. Во время некроза из этих клеток (после повреждения ткани или повреждения клеток) экспрессия IL-33 увеличивается, и он высвобождается во внеклеточное пространство и действует как сигнал эндогенной опасности, отправляя предупреждающие сигналы на соседние клетки и ткани. В последнее время появилось много исследований, в которых показано, что IL-33 может участвовать в механизме развития и прогрессирования фиброза различных органов, но при этом оказывает противовоспалительное действие на механизмы развития других заболеваний. В данном обзоре будут обсуждаться биологические характеристики IL-33 и роль сигнального пути IL-33/ST2 в развитии фиброза.</p></abstract><trans-abstract xml:lang="en"><p>Interleukin 33 (IL-33) is a member of the IL-1 family, which is widely expressed on all types of cells. IL-33 was identified as a functional ligand for the plasma membrane receptor complex, which is a heterodimer consisting of a membrane bound ST2 receptor (growth stimulating factor). IL-33 is involved in the development of immune response with predominant release of pro-inflammatory T helper type 2 cytokines. IL-33 is widely expressed on various structure-forming cells, such as epithelial, endothelial and smooth muscle cells. Increased expression of IL-33 is observed during necrosis of these cells (after tissue or cell damage), and it is released into extracellular space, and acts as an endogenous danger signal, sending a sort of warnings to neighboring cells and tissues. Recently, many studies have shown that IL-33 can participate in development and progression of fibrosis in various organs. However, it exerts anti-inflammatory effects upon development of other diseases. This review will discuss biological characteristics of IL-33 and a role of the IL-33/ST2 signaling pathway in the development of fibrosis. </p></trans-abstract><kwd-group xml:lang="ru"><kwd>интерлейкин-33</kwd><kwd>фиброз</kwd><kwd>стимулирующий фактор роста</kwd></kwd-group><kwd-group xml:lang="en"><kwd>interleukin 33</kwd><kwd>fibrosis</kwd><kwd>growth-stimulating factor</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">Ashlin T.G., Buckley M.L., Salter R.C., Johnson J.L., Kwan A.P., Ramji D.P. The anti-atherogenic cytokine interleukin-33 inhibits the expression of a disintegrin and metalloproteinase with thrombospondin motifs-1, -4 and -5 in human macrophages: Requirement of extracellular signal-regulated kinase, c-Jun N-terminal kinase and phosphoinositide 3-kinase signaling pathways. Int. J. Biochem. 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