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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">rsp</journal-id><journal-title-group><journal-title xml:lang="ru">Научно-практическая ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Rheumatology Science and Practice</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1995-4484</issn><issn pub-type="epub">1995-4492</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1995-4484-2017-68-86</article-id><article-id custom-type="elpub" pub-id-type="custom">rsp-2341</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>ПРОГРЕСС В РЕВМАТОЛОГИИ В XXI ВЕКЕ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>PROGRESS IN RHEUMATOLOGY IN THE XXI CENTURY</subject></subj-group></article-categories><title-group><article-title>Новые возможности фармакотерапии иммуновоспалительных ревматических заболеваний: фокус на ингибиторы интерлейкина 17</article-title><trans-title-group xml:lang="en"><trans-title>NEW POSSIBILITIES OF PHARMACOTHERAPY FOR IMMUNOINFLAMMATORY RHEUMATIC DISEASES: A FOCUS ON INHIBITORS OF INTERLEUKIN-17</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>Насонов</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Nasonov</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>научный руководитель ФГБНУ НИИР им. В.А. Насоновой, заведующий кафедрой ревматологии ИПО ГБОУ ВПО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России, академик РАН, профессор, докт. мед. наук</p><p>115522 Москва, Каширское шоссе, 34А</p><p>119991 Москва, ул. Трубецкая, 8, стр. 2</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p><p>8, Trubetskaya St., Build. 2, Moscow 119991 Department of Rheumatology</p></bio><email xlink:type="simple">nasonov@irramn.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им.  В.А. Насоновой»&#13;
&#13;
ФГБОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology&#13;
&#13;
Institute of Professional Education, I.M. Sechenov First Moscow State Medical  University, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>08</day><month>03</month><year>2017</year></pub-date><volume>55</volume><issue>1</issue><fpage>68</fpage><lpage>86</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Насонов Е.Л., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Насонов Е.Л.</copyright-holder><copyright-holder xml:lang="en">Nasonov E.L.</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://rsp.mediar-press.net/rsp/article/view/2341">https://rsp.mediar-press.net/rsp/article/view/2341</self-uri><abstract><p>В последние годы большое внимание привлечено к Th17-клеткам, синтезирующим интерлейкин 17 (ИЛ17), в отличие от Th1- и Th2-клеток, «маркерными» цитокинами которых являются соответственно интерферон γ (ИФНγ) и ИЛ4. Полагают, что именно патологическая активация и экспансия Th17-клеток играют ведущую роль в развитии широкого спектра иммуновоспалительных заболеваний (ИВЗ) человека, включая ревматоидный артрит (РА), псориаз, анкилозирующий спондилит (АС), псориатический артрит (ПсА), воспалительные заболевания кишечника, системную красную волчанку, которые ранее рассматривались как Th1-зависимые заболевания, связанные в первую очередь с гиперпродукцией ИЛ2 и ИФНγ. Это послужило мощным стимулом для разработки новых генно-инженерных биологических препаратов, механизм действия которых основан на блокировании патологических эффектов ИЛ17, других связанных с активацией Th17-клеток цитокинов, или «малых молекул», интерферирующих с факторами транскрипции, регулирующими синтез этих цитокинов. В обзоре обсуждаются современные исследования, касающиеся механизмов регуляции образования и функциональной активности цитокинов семейства ИЛ17, и доказательства значения этих цитокинов в патогенезе ИВЗ. Особое внимание уделяется клинической эффективности и безопасности моноклональных антител к ИЛ17А – препарату секукинумаб – при псориазе, ПсА, АС и РА.</p></abstract><trans-abstract xml:lang="en"><p>In recent years, more attention has been focused on Th17 cells that synthesize interleukin-17 (IL-17) in contrast to Th1 and Th2 cells, the marker cytokines of which are interferon-γ (IFN-γ) and IL-4, respectively. It is precisely these pathological activation and expansion of Th17 cells that are supposed to play a key role in the development of a wide spectrum of human immunoinflammatory diseases (IIDs), including rheumatoid arthritis (RA), psoriasis, ankylosing spondylitis (AS), psoriatic arthritis (PsA), inflammatory bowel disease, and systemic lupus erythematosus, which were previously considered as Th1-dependent diseases associated primarily with the hyperproduction of IL-2 and IFN-γ. This has served as a powerful stimulus to design new biological agents, the mechanism of action of which is based on blocking the pathological effects of IL-17, others associated with the activation of Th17 cells of cytokines, or small molecules interfering with transcription factors that regulate the synthesis of these cytokines. This review discusses current studies of the mechanisms regulating the formation and functional activity of IL-17 family cytokines, as well as evidence of the importance of these cytokines in the pathogenesis of IIDs. Special attention is paid to the clinical efficacy and safety of anti-IL-17A monoclonal antibody secukinumab used to treat psoriasis, PsA, AS, and RA.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ось ИЛ17/ИЛ23</kwd><kwd>интерлейкин 17</kwd><kwd>псориаз</kwd><kwd>псориатический артрит</kwd><kwd>анкилозирующий спондилит</kwd><kwd>ревматоидный артрит</kwd></kwd-group><kwd-group xml:lang="en"><kwd>IL-17/IL-23 axis</kwd><kwd>interleukin 17</kwd><kwd>psoriasis</kwd><kwd>psoriatic arthritis</kwd><kwd>ankylosing spondylitis</kwd><kwd>rheumatoid arthritis</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">Mosmann TR, Coffman RL. 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