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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-FIC-2385</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-2385</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>ОРИГИНАЛЬНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES</subject></subj-group></article-categories><title-group><article-title>Уровень экспрессии генов FOXP3, IL2R, CD8A, RORγ в лейкоцитах периферической крови здоровых людей и пациентов с артериальной гипертензией</article-title><trans-title-group xml:lang="en"><trans-title>FOXP3, IL2R, CD8A and RORγ gene expression in peripheral blood leukocytes of healthy people and patients with arterial hypertension</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8697-2086</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Топчиева</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Topchieva</surname><given-names>L. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Топчиева Людмила Владимировна – кандидат биологических наук, ведущий научный сотрудник лаборатории генетики, Институт биологии – обособленное подразделение</p><p>185910, Республика Карелия, г. Петрозаводск, ул. Пушкинская, 11</p></bio><bio xml:lang="en"><p>Topchieva Ludmila V., PhD (Biology), Leading Research Associate, Laboratory of Genetics</p><p>185910, Republic of Karelia, Petrozavodsk, Pushkinskaya str., 11</p></bio><email xlink:type="simple">topchieva67@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2231-4695</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Корнева</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Korneva</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Корнева Виктория Алексеевна – кандидат медицинских наук, доцент кафедры факультетской терапии, фтизиатрии, инфекционных болезней и эпидемиологии, Медицинский институт</p><p>Республика Карелия, г. Петрозаводск</p><p> </p></bio><bio xml:lang="en"><p>Korneva Viktoria A., PhD (Medicine), Associate Professor, Department of Faculty Therapy, Phthisiology, Infectious Diseases and Epidemiology, Medical Institute</p><p>Republic of Karelia, Petrozavodsk</p><p> </p></bio><email xlink:type="simple">vikkorneva@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/0000-0003-3583-0218</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Малышева</surname><given-names>И. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Malysheva</surname><given-names>I. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Малышева Иртна Евгеньевна – кандидат биологических наук, старший научный сотрудник лаборатории генетики</p><p>Республика Карелия, г. Петрозаводск</p></bio><bio xml:lang="en"><p>Malysheva Irina E., PhD (Biology), Senior Research Associate, Laboratory of Genetics</p><p>Republic of Karelia, Petrozavodsk</p><p> </p></bio><email xlink:type="simple">i.e.malysheva@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Институт биологии – обособленное подразделение ФГБУН «Федеральный исследовательский центр “Карельский научный центр Российской академии наук”»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Biology, Karelian Research Centre, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБОУ ВО «Петрозаводский государственный университет»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Petrozavodsk State University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>20</day><month>04</month><year>2022</year></pub-date><volume>24</volume><issue>2</issue><fpage>273</fpage><lpage>282</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Топчиева Л.В., Корнева В.А., Малышева И.Е., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Топчиева Л.В., Корнева В.А., Малышева И.Е.</copyright-holder><copyright-holder xml:lang="en">Topchieva L.V., Korneva V.A., Malysheva I.E.</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/2385">https://www.mimmun.ru/mimmun/article/view/2385</self-uri><abstract><p>Нарушение баланса Т-регуляторных и Т-эффекторных лимфоцитов рассматривается в последнее время как важное патогенетическое звено артериальной гипертензии (АГ). Однако данные литературы относительно количества этих клеток у пациентов с АГ или у экспериментальных животных с разными моделями индуцированной гипертензии противоречивые. Основные сведения об изменении паттерна иммунных клеток при сердечно-сосудистых заболеваниях получены с использованием проточной цитометрии. В литературе встречаются также данные об экспрессии у больных c патологиями сердечно-сосудистой системы генов, кодирующих поверхностные и цитоплазматические дифференцировочные антигены иммунных клеток, которые совпадают с результатами исследований, полученных с помощью проточной цитометрии. Цель исследования: анализ уровня транскриптов генов, кодирующих маркеры дифференцировки регуляторных (FOXP3, IL2R) и эффекторных Т-лимфоцитов (Т-хелперов 17 (RORγ) и СD8 лимфоцитов (CD8A) у здоровых людей и пациентов с артериальной гипертензией (I-II стадии). Обследованы здоровые индивиды (40 человек, 20 мужчин и 20 женщин), пациенты с АГ, не принимавшие гипотензивные препараты (27 человек, 14 мужчин и 13 женщин), пациенты с АГ, принимающие блокаторы β-адренорецепторов (метопролол или бисопролол) (26 человек, 12 мужчин и 14 женщин). Относительный уровень транскриптов в лейкоцитах периферической крови оценивали методом ОТ-ПЦР в режиме реального времени. Показано, что транскрипционная активность FOXP3, IL2R, RORγ и CD8A генов в лейкоцитах периферической крови больных людей существенно выше, чем у здоровых индивидов (p &lt; 0,01). Это, вероятно, свидетельствует о повышении у гипертоников количества циркулирующих Т-регуляторных лимфоцитов, CD8+ клеток и T-хелперов 17 и активации у них Т-клеточного иммунитета. Статистически значимых различий в содержании мРНК генов FOXP3, IL2R, RORγ и CD8A в лейкоцитах периферической крови мужчин и женщин, как в группе здоровых людей, так и группе пациентов с АГ не выявлено. На фоне приема кардиоселективных блокаторов β-адренорецепторов (метопролола и бисопролола) у гипертоников наблюдался более низкий уровень экспрессии указанных генов, что, вероятно, указывает на противовоспалительные и иммуномодулирующие свойства этих препаратов.</p><p> </p></abstract><trans-abstract xml:lang="en"><p>Impaired balance of T regulatory and T effector lymphocytes has recently been considered as an important pathogenetic link in arterial hypertension (AH). There are, however, contradictory literature data about contents of these cells in the patients with hypertension, or obtained in experimental animal models of induced hypertension. Most results about changed patterns of immune cells in cardiovascular diseases were obtained by means of flow cytometry. There are also some works on expression of genes encoding surface and cytoplasmic differentiation antigens of immune cells in the patients with cardiovascular pathologies. These results coincide with the data obtained with flow cytometric techniques. Purpose of the present study was to analyze of the levels of gene transcripts encoding differentiation markers of regulatory (FOXP3, IL2R) T cells, effector T subpopulations (T helpers 17 (RORγ), and CD8 lymphocytes (CD8A) in healthy subjects and the patients with arterial hypertension (stages I-II). We examined healthy individuals (40 people, 20 men and 20 women), 27 patients with hypertension who did not receive antihypertensive therapy (14 men and 13 women), 26 hypertensive patients taking β-adrenergic receptor blockers (metoprolol or bisoprolol), including 12 men and 14 women. The relative levels of transcripts in peripheral blood leukocytes were assessed by real-time RT-PCR. It was shown that the transcriptional activity of FOXP3, IL2R, RORγ, and CD8A genes in peripheral blood leukocytes of the diseased people was significantly higher than in healthy individuals (p &lt; 0.01). This finding may indicate an increased number of circulating T regulatory lymphocytes, CD8+ cells and T helpers 17 in hypertensive patients, and activation of T cell immunity in these patients. There were no statistically significant gender differences in FOXP3, IL2R, RORγ and CD8A gene expression in leukocytes, both in the group of healthy people and in hypertensive patients. The patients receiving cardioselective β-adrenergic receptor blockers (metoprolol and bisoprolol) exhibited lower expression of these genes, thus, probably, indicating antiinflammatory and immunomodulatory properties of these drugs.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>артериальная гипертензия</kwd><kwd>адаптивный иммунитет</kwd><kwd>Т-регуляторные лимфоциты</kwd><kwd>Т-эффекторные лимфоциты</kwd><kwd>экспрессия генов</kwd><kwd>кардиоселективные блокаторы β-адренорецепторов</kwd></kwd-group><kwd-group xml:lang="en"><kwd>arterial hypertension</kwd><kwd>adaptive immunity</kwd><kwd>T regulatory lymphocytes</kwd><kwd>T effector lymphocytes</kwd><kwd>gene expression</kwd><kwd>β-adrenergic receptor blockers</kwd><kwd>cardioselective</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследования выполнялись в рамках выполнения НИР (№ 0218-2019-0077) ИБ КарНЦ РАН на научном оборудовании (НО) Центра коллективного пользования Федерального исследовательского центра «Карельский научный центр Российской академии наук»</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Трушина Э.Н., Мустафина О.К., Хорхе С.С., Богданов А.Р., Сенцова Т.Б., Залетова Е.С., Кузнецов В.Д. 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