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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">10.15789/1563-0625-2019-3-407-418</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-1814</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>ИММУНОЛОГИЧЕСКИЕ АСПЕКТЫ ЭССЕНЦИАЛЬНОЙ ГИПЕРТЕНЗИИ</article-title><trans-title-group xml:lang="en"><trans-title>IMMUNOLOGICAL ASPECTS OF ESSENTIAL HYPERTENSION</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>Тимашева</surname><given-names>Я. Р.</given-names></name><name name-style="western" xml:lang="en"><surname>Timasheva</surname><given-names>Ya. R.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., научный сотрудник лаборатории физиологической генетики, (450054, Республика Башкортостан, г. Уфа, пр. Октября, 71, тел./факс: 8 (347) 235-60-88);</p><p>доцент кафедры медицинской генетики и фундаментальной медицины ИДПО.</p></bio><bio xml:lang="en"><p>PhD (Medicine), Research Associate, Laboratory of Physiological Genetics (450054, Republic of Bashkortostan, Ufa, October ave., 71, Phone/Fax: 7 (347) 235-60-88);</p><p>Associate Professor at the Department of Medical Genetics and Fundamental Medicine.</p></bio><email xlink:type="simple">ianina_t@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Институт биохимии и генетики Уфимского федерального исследовательского центра Российской академии наук; ФГБОУ ВО «Башкирский государственный медицинский университет»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Biochemistry and Genetics, Ufa Federal Research Center, Russian Academy of Sciences; Bashkir State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>11</day><month>07</month><year>2019</year></pub-date><volume>21</volume><issue>3</issue><fpage>407</fpage><lpage>418</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Тимашева Я.Р., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Тимашева Я.Р.</copyright-holder><copyright-holder xml:lang="en">Timasheva Y.R.</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/1814">https://www.mimmun.ru/mimmun/article/view/1814</self-uri><abstract><p>Согласно современным представлениям об этиопатогенезе эссенциальной гипертензии, важная роль в ее развитии принадлежит клеткам иммунной системы. Медиаторы, продуцируемые иммунокомпетентными клетками, принимают участие в возникновении и поддержании состояния хронического системного воспаления и способствуют развитию сосудистого ремоделирования, являющегося важным звеном патогенеза заболевания и поражения органов-мишеней. Иммунные механизмы, лежащие в основе повышения артериального давления, включают в себя активацию клеток врожденного и приобретенного иммунитета. Нарушение целостности эндотелия сосудов, запускающее каскад воспалительных реакций, вызывает миграцию в очаг повреждения клеток иммунной системы, привлеченных хемокинами и молекулами адгезии. Инфильтрация макрофагами периваскулярной ткани способствует нарушению вазодилатации и повреждению органов-мишеней благодаря выработке активных форм кислорода. Ангиотензин II вызывает также инфильтацию периваскулярной жировой ткани и адвентиции Т-лимфоцитами и повышенную выработку фактора некроза опухолей альфа и интерферона гамма. Кроме того, Т-лимфоциты экспрессируют минералокортикоидный рецептор, участвующий в развитии системной гипертензии. Важная роль в прогрессировании гипертензии принадлежит интерлейкину-17, участвующему в развитии повышенного артериального давления и ремоделирования сосудов. В обзоре также представлены данные о влиянии кишечной микрофлоры на регуляцию артериального давления и развитие гипертензии.</p></abstract><trans-abstract xml:lang="en"><p>According to modern concept of the etiopathogenesis of essential hypertension, immune cells play an important role in its development. Mediators produced by immunocompetent cells participate in the initiation and maintenance of chronic systemic inflammation and promote the development of vascular remodeling which is an important part of the pathogenesis of the disease and target organ damage. The immune mechanisms underlying blood pressure elevation include the activation of innate and adaptive immune cells. Endothelial damage triggers an inflammatory cascade, causing migration of the immune cells to the inflammatory site, mediated by chemokines and adhesion molecules. Macrophage infiltration of perivascular tissue contributes to impaired vasodilation and damage to target organs due to the production of active forms of oxygen. Angiotensin II also causes T cell infiltration of perivascular adipose tissue and adventitia and an increased production of tumor necrosis factor alpha and interferon gamma. In addition, T lymphocytes express the mineralocorticoid receptor involved in the development of systemic hypertension. An important role in the progression of hypertension belongs to interleukin-17, which is involved in blood pressure elevation and vascular remodeling. The review also contains data on the effect of gut microbiota on the regulation of blood pressure and the development of hypertension.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>эссенциальная гипертензия</kwd><kwd>артериальное давление</kwd><kwd>воспаление</kwd><kwd>цитокины</kwd><kwd>хемокины</kwd><kwd>Т-лимфоциты</kwd></kwd-group><kwd-group xml:lang="en"><kwd>essential hypertension</kwd><kwd>blood pressure</kwd><kwd>inflammation</kwd><kwd>cytokines</kwd><kwd>chemokines</kwd><kwd>T cells</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">Ba D., Takeichi N., Kodama T., Kobayashi H. Restoration of T cell depression and suppression of blood pressure in spontaneously hypertensive rats (SHR) by thymus grafts or thymus extracts. J. Immunol., 1982, Vol. 128, no. 3, p. 1211.</mixed-citation><mixed-citation xml:lang="en">Ba D., Takeichi N., Kodama T., Kobayashi H. 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