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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">mrj</journal-id><journal-title-group><journal-title xml:lang="ru">Современная ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Modern Rheumatology Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1996-7012</issn><issn pub-type="epub">2310-158X</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1996-7012-2018-1-55-59</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-809</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>Регуляторы роста паннуса при ревматоидном артрите, являющиеся потенциальными мишенями биологической терапии</article-title><trans-title-group xml:lang="en"><trans-title>Pannus growth regulators as potential targets for biological therapy in rheumatoid arthritis</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>Михайлова</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Mikhaylova</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>620028, Екатеринбург, ул. Репина, 3</p></bio><bio xml:lang="en"><p>3, Repin St., Yekaterinburg 620028</p></bio><email xlink:type="simple">mikhaylovamail@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>Лесняк</surname><given-names>О. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Lesnyak</surname><given-names>O. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>191015, Санкт-Петербург, ул. Кирочная, 41</p></bio><bio xml:lang="en"><p>41, Kirochnaya St., Saint Petersburg 191015</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Уральский государственный медицинский университет» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Ural State Medical University, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБОУ ВО «Северо-Западный государственный медицинский университет им.  И.И. Мечникова» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.I. Mechnikov North-Western State Medical&#13;
University, Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>02</day><month>04</month><year>2018</year></pub-date><volume>12</volume><issue>1</issue><fpage>55</fpage><lpage>59</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Михайлова А.С., Лесняк О.М., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Михайлова А.С., Лесняк О.М.</copyright-holder><copyright-holder xml:lang="en">Mikhaylova A.S., Lesnyak O.M.</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://mrj.ima-press.net/mrj/article/view/809">https://mrj.ima-press.net/mrj/article/view/809</self-uri><abstract><p>Основной целью лечения ревматоидного артрита (РА) является подавление воспаления с помощью базисной и симптоматической терапии. При этом указанная стратегия значимо не  останавливает деструкцию сустава, ведущую к инвалидизации пациентов. В обзоре  представлен анализ публикаций, посвященных поиску регуляторов межклеточного  взаимодействия среди основных эффекторных клеток паннуса – фибробластоподобных  синовиоцитов (ФПС). Представлены оценка влияния факторов агрессии ФПС на инвазивное  «поведение» паннуса, возможность их прицельной дезактивации в рамках биологической  терапии, а также предварительные результаты подобного лечения на примерах животных  моделей. Показано, что наиболее перспективными мишенями биологической терапии могут  являться молекулы адгезии ФПС: трансмембранный рецептор кадгерин 11, интегрины α5/β1, VCAM1, ICAM1, активно участвующие в процессах прикрепления ФПС к поверхности хряща  и активирующие выработку ими цитокинов, факторов роста и агрессии.</p></abstract><trans-abstract xml:lang="en"><p>The main goal of treatment for rheumatoid arthritis (RA) is to suppress inflammation using basic and symptomatic therapies. At the same time, the above strategy does not significantly stop joint  destruction that leads to disability in patients. The review analyzes  publications dealing with a search for intercellular interaction  regulators among the main effector cells in the pannus – fibroblast- like synoviocytes (FLSs). It assesses the influence of FLS aggression  factors on invasive pannus behavior, the possibility of their targeted deactivation during biological therapy, and the preliminary  results of similar treatment by the examples of animal models. It is  shown that the most promising targets for biological therapy may be FLS adhesion molecules, such as transmembrane receptor cadherin  11, integrins α5/β1, and VCAM1, ICAM1, which actively participate in the attachment of FLSs to the cartilage surface and activate their production of cytokines, growth factors and aggression factors.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ревматоидный артрит</kwd><kwd>паннус</kwd><kwd>фибробластоподобные синовиоциты</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rheumatoid arthritis</kwd><kwd>pannus</kwd><kwd>fibroblast-like synoviocytes</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">Чичасова НВ. Деструкция хряща при ревматоидном артрите, связь с функциональными нарушениями. Современная ревматология. 2014;8(4):60–71. [Chichasova NV. 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