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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">ateroskleroz</journal-id><journal-title-group><journal-title xml:lang="ru">Атеросклероз</journal-title><trans-title-group xml:lang="en"><trans-title>Ateroscleroz</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2078-256X</issn><issn pub-type="epub">2949-3633</issn><publisher><publisher-name>НИИТПМ-филиал ИЦиГ СО РАН</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">ateroskleroz-751</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>Клетки-супрессоры – основа иммунопатогенеза атеросклероза</article-title><trans-title-group xml:lang="en"><trans-title>The suppressor cells – the basis of immunopathogenesis of atherosclerosis</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>Козлов</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kozlov</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Владимир Александрович Козлов, д-р мед. наук, академик, директор</p><p>630099</p><p>ул. Ядринцевская, 14</p><p>Новосибирск</p></bio><bio xml:lang="en"><p>630099</p><p>Yadrintsevskaya str., 14</p><p>Novosibirsk</p></bio><email xlink:type="simple">vakoz40@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «НИИ фундаментальной и клинической иммунологии»</institution></aff><aff xml:lang="en"><institution>Scientific Research Institute of Fundamental and Clinical Immunology</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>17</day><month>04</month><year>2022</year></pub-date><volume>11</volume><issue>2</issue><fpage>37</fpage><lpage>42</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Козлов В.А., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Козлов В.А.</copyright-holder><copyright-holder xml:lang="en">Kozlov V.A.</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://ateroskleroz.elpub.ru/jour/article/view/751">https://ateroskleroz.elpub.ru/jour/article/view/751</self-uri><abstract><p>   Атеросклероз является сосудистым заболеванием, в процессе формирования которого принимают участие иммунокомпетентные клетки (макрофаги, дендритные клетки, лимфоциты), эндотелиальные и гладкомышечные клеточные элементы во взаимодействии с липопротеинами, обогащенными холестеролом. При этом циркулирующие CD4+ Т-лимфоциты дифференцируются преимущественно в клетки Th1, которые реагируют на специфические антигены, такие как окисленные липопротеины низкой плотности и белки теплового шока (HSP60/65), индуцируя процессы повреждения эндотелия и гладкомышечных клеток. Вопрос о том, будет ли развиваться атеросклероз и любое другое заболевание с иммунопатогенетической основой, зависит от сбалансированного участия в процессе регуляторных клеток с супрессорной активностью, в частности, CD4+CD25+Foxp3+ Treg. Многочисленные данные свидетельствуют о снижении содержания Treg у больных атеросклерозом и уменьшении их супрессорной активности. Все терапевтические воздействия, стимулирующие активность Treg, положительно влияют на течение экспериментального атеросклероза.</p></abstract><trans-abstract xml:lang="en"><p>   Atherosclerosis is a vascular disease, in the formation of which is attended immunocompetent cells (macrophages, dendritic cells, lymphocytes), endothelial and smooth muscle cell elements in interaction with the lipoprotein enriched with cholesterol. Thus, circulating CD4+ T lymphocytes are differentiated mainly in Th1 cells that respond to specific antigens, such as oxidized LDL and heat shock proteins (HSP60/65) induces the processes of endothelial damage and smooth muscle cells). The question that will or will not develop atherosclerosis depends on balanced participation in the process regulatory cells with suppressor activity, in particular CD4+CD25+Foxp3+ Treg. Numerous data suggest about the reduction of Treg in patients with atherosclerosis and reducing their suppressor activity. All therapeutic effects of stimulating the activity of Treg positively influence the course of experimental atherosclerosis.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>атеросклероз</kwd><kwd>иммунологическая толерантность</kwd><kwd>иммунокомпетентные клетки с супрессорной активностью</kwd></kwd-group><kwd-group xml:lang="en"><kwd>immunopathogenesis of atherosclerosis</kwd><kwd>immunological tolerance</kwd><kwd>immunocompetence cells with suppressor activity</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">Zhou X., Nicolleti A., Elhage R., Hansson G. K. Transfer of CD4+ T cells aggravates atherosclerosis in immunodeficient apolipoprotein E knockout mice // Circulation. 2000. Vol. 102. P. 2919–2922.</mixed-citation><mixed-citation xml:lang="en">Zhou X., Nicolleti A., Elhage R., Hansson G. K. 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