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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">10.14412/1995-4484-2016-60-77</article-id><article-id custom-type="elpub" pub-id-type="custom">rsp-2171</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>Роль интерлейкина 1 в развитии заболеваний человека</article-title><trans-title-group xml:lang="en"><trans-title>ROLE OF INTERLEUKIN 1 IN THE DEVELOPMENT OF HUMAN 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>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>директор ФГБНУ НИИР им. В.А. Насоновой, академик РАН, докт. мед. наук, профессор,</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</p></bio><email xlink:type="simple">sokrat@irramn.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>Елисеев</surname><given-names>М. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Eliseev</surname><given-names>M. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>зав. лабораторией микрокристаллических артритов, канд. мед. наук,</p><p>115522 Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ Научно-исследовательский институт ревматологии им. В.А. Насоновой;&#13;
ГБОУ ВПО «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;
I.M. Sechenov First Moscow State Medical University, Ministry of Health of&#13;
Russia</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБНУ Научно-исследовательский институт ревматологии им. В.А. Насоновой</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>23</day><month>03</month><year>2016</year></pub-date><volume>54</volume><issue>1</issue><fpage>60</fpage><lpage>77</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Насонов Е.Л., Елисеев М.С., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Насонов Е.Л., Елисеев М.С.</copyright-holder><copyright-holder xml:lang="en">Nasonov E.L., Eliseev M.S.</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/2171">https://rsp.mediar-press.net/rsp/article/view/2171</self-uri><abstract><p>Иммуновоспалительные заболевания человека в зависимости от преобладающих механизмов активации иммунитета разделяются на две основные категории: аутоиммунные и аутовоспалительные. В то же время между аутоиммунными и аутовоспалительными заболеваниями много общего в отношении как спектра клинических проявлений, так и «триггерных» внешнесредовых, эпигенетических и генетических факторов, медиаторов воспаления, тканевого повреждения и подходов к фармакотерапии. Предполагается, что гиперпродукция «провоспалительного» цитокина – интерлейкина 1 (ИЛ1) – во многом определяет «перекрест» между аутоиммунитетом и аутовоспалением, характерный для многих иммуновоспалительных заболеваний. Изучение роли ИЛ1 в регуляции взаимодействия между врожденным (активация Toll-подобных рецепторов, инфламмасомы) и приобретенным (Th1- и Th17-типы иммунного ответа) иммунитетом и эффективности ингибиторов ИЛ1 может иметь важное значение в плане расшифровки патогенетических механизмов иммуно-воспалительных заболеваний человека и разработки новых подходов к персонифицированной терапии.</p></abstract><trans-abstract xml:lang="en"><p>According to the predominant mechanisms of immunity activation, human inflammatory diseases are divided into two main categories: autoimmune and autoinflammatory ones. At the same time, the autoimmune and autoinflammatory diseases have much common in both the range of clinical manifestations and trigger environmental, epigenetic, and genetic factors, inflammatory mediators, tissue damage, and approaches to pharmacotherapy. The hyperproduction of the proinflammatory cytokine interleukin 1 (IL-1) is supposed to largely determine the cross between autoimmunity and autoinflammation, which is characteristic of many immunoinflammatory diseases. The study of a role of IL-1 in regulating an interaction between innate (Toll-like receptor activation, inflammasomes) and adaptive (Th1 and Th17 immune responses) immunities and efficiency of IL-1 inhibitors may be of great importance in interpreting the pathogenetic mechanisms of human immunoinflammatory diseases and elaborating novel approaches to personified therapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>иммуновоспалительные заболевания</kwd><kwd>аутовоспалительные заболевания</kwd><kwd>цитокины</kwd><kwd>ин- фламмасома</kwd><kwd>интерлейкин 1</kwd><kwd>ингибиторы интерлейкина 1</kwd></kwd-group><kwd-group xml:lang="en"><kwd>immunoinflammatory diseases</kwd><kwd>autoinflammatory diseases</kwd><kwd>cytokines</kwd><kwd>inflammasome</kwd><kwd>interleukin 1</kwd><kwd>interleukin 1 inhibitors</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">McGonagle D, McDermott MF. 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