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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">nogr</journal-id><journal-title-group><journal-title xml:lang="ru">Экспериментальная и клиническая гастроэнтерология</journal-title><trans-title-group xml:lang="en"><trans-title>Experimental and Clinical Gastroenterology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1682-8658</issn><publisher><publisher-name>«Global Media Technologies»</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">nogr-461</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>ЛЕКЦИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LECTION</subject></subj-group></article-categories><title-group><article-title>РОЛЬ МИКРОБИОТЫ В ФОРМИРОВАНИИ АУТОИММУННОГО ВОСПАЛЕНИЯ ПРИ ВОСПАЛИТЕЛЬНЫХ ЗАБОЛЕВАНИЯХ КИШЕЧНИКА</article-title><trans-title-group xml:lang="en"><trans-title>THE ROLE OF MICROBIOTA IN DEVELOPMENT OF AUTOIMMUNE INFLAMMATION IN INFLAMMATORY BOWEL DISEASES</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>Данилова</surname><given-names>Н. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Danilova</surname><given-names>N. A.</given-names></name></name-alternatives><email xlink:type="simple">danilova.natalya.87@mail.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>Валеева</surname><given-names>А. Р.</given-names></name><name name-style="western" xml:lang="en"><surname>Valeeva</surname><given-names>A. R.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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>Абдулхаков</surname><given-names>С. Р.</given-names></name><name name-style="western" xml:lang="en"><surname>Abdulkhakov</surname><given-names>S. R.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Скороходкина</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Skorokhodkina</surname><given-names>O. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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>Абдулхаков</surname><given-names>Р. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Abdulkhakov</surname><given-names>R. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Казанский государственный медицинский университет<country>Россия</country></aff><aff xml:lang="en">Kazan State Medical University<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">Казанский государственный медицинский университет; Казанский федеральный университет<country>Россия</country></aff><aff xml:lang="en">Kazan State Medical University; Kazan Federal University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>20</day><month>07</month><year>2017</year></pub-date><volume>0</volume><issue>7</issue><fpage>121</fpage><lpage>125</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Данилова Н.А., Валеева А.Р., Абдулхаков С.Р., Скороходкина О.В., Абдулхаков Р.А., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Данилова Н.А., Валеева А.Р., Абдулхаков С.Р., Скороходкина О.В., Абдулхаков Р.А.</copyright-holder><copyright-holder xml:lang="en">Danilova N.A., Valeeva A.R., Abdulkhakov S.R., Skorokhodkina O.V., Abdulkhakov R.A.</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.nogr.org/jour/article/view/461">https://www.nogr.org/jour/article/view/461</self-uri><abstract><p>Изучение роли генетических факторов, кишечной микробиоты и состояния иммунной системы в патогенезе воспалительных заболеваний кишечника обусловлено продолжающимся ростом заболеваемости язвенным колитом и болезнью Крона, неизвестной этиологией, недостаточно изученным патогенезом данных заболеваний и недостаточной эффективностью существующих методов лечения. В последние годы широко обсуждается роль генетических факторов, детерминирующих предрасположенность к развитию аутоиммунных реакций, приводящих к формированию хронического воспаления, а также ассоциации генетических факторов и определенного состава кишечной микробиоты в патогенезе воспалительных заболеваний кишечника. Изменения кишечного микробиома рассматриваются в качестве одного из триггеров формирования аутоиммунного воспаления. При этом ключевым дефектом, предрасполагающим к развитию воспалительных заболеваний кишечника, является нарушение распознавания бактериальных молекулярных маркеров дендритными клетками, что приводит к активации Th1, Th2 и Th17 адаптивных субпопуляций лимфоцитов. Не исключается, что именно особенности состава кишечной микробиоты могут быть причиной индукции хронического аутоиммунного воспаления при воспалительных заболеваниях кишечника.</p></abstract><trans-abstract xml:lang="en"><p>The continuous study of the role of genetic factors, intestinal microbiota, and immune system in the pathogenesis of inflammatory bowel diseases is due to the ongoing increase of incidences of ulcerative colitis and Crohn’s disease, unknown etiology, and insufficiently studied pathogenesis of these diseases, as well as insufficient efficiency of existing treatment methods. The role of genetic factors determining predisposition to autoimmune reactions leading to chronic inflammation as well as association of genetic factors and particular composition of intestinal microbiota in pathogenesis of inflammatory bowel diseases are discussed recently. Changes of intestinal microbiome are considered to be one of the triggers of autoimmune inflammation. Violation of recognition of bacterial molecular markers by dendritic cells, leading to activation of Th1, Th2 and Th17 lymphocytes adaptive subpopulations is considered to be the key defect predisposing to inflammatory bowel diseases development. Probably it is the peculiarities of the composition of the intestinal microbiota that can be the cause of chronic autoimmune inflammation induction in inflammatory bowel diseases.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>микробиота</kwd><kwd>цитокины</kwd><kwd>язвенный колит</kwd><kwd>болезнь Крона</kwd><kwd>воспалительные заболевания кишечника</kwd></kwd-group><kwd-group xml:lang="en"><kwd>microbiota</kwd><kwd>cytokines</kwd><kwd>ulcerative colitis</kwd><kwd>Crohn’s disease</kwd><kwd>inflammatory bowel diseases</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">Loddo I, Romano C. 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