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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">10.15789/1563-0625-2005-4-347-354</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-467</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>РЕГУЛЯТОРНЫЕ Т–КЛЕТКИ: ПРОИСХОЖДЕНИЕ И ФУНКЦИИ</article-title><trans-title-group xml:lang="en"><trans-title>REGULATORY T–CELLS: ORIGIN AND FUNCTION</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>Фрейдлин</surname><given-names>И. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Freidlin</surname><given-names>I. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Отдел иммунологии </p><p>197376, Санкт–Петербург, ул .Акад. Павлова, д. 12</p></bio><email xlink:type="simple">irinaf@spmu.rssi.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>НИИ экспериментальной медицины РАМН, Санкт–Петербург</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2005</year></pub-date><pub-date pub-type="epub"><day>22</day><month>07</month><year>2014</year></pub-date><volume>7</volume><issue>4</issue><fpage>347</fpage><lpage>354</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Фрейдлин И.С., 2014</copyright-statement><copyright-year>2014</copyright-year><copyright-holder xml:lang="ru">Фрейдлин И.С.</copyright-holder><copyright-holder xml:lang="en">Freidlin I.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://www.mimmun.ru/mimmun/article/view/467">https://www.mimmun.ru/mimmun/article/view/467</self-uri><abstract><p>Резюме. За последние 10 лет предупреждение аутоиммунных заболеваний стали связывать с популяцией так называемых регуляторных Т клеток (Treg клеток). В данном обзоре обсуждаются молекулярные механизмы развития и функций Treg клеток, включая идентификацию уникального молекулярного маркера Treg клеток – фактора транскрипции – Foxp3. Обсуждаются также механизмы супрессии, к которым относятся прямые контакты через связывание поверхностных молекул CTLA–4 на Treg клетках с CD80/CD86 молекулами на эффекторных Т–клетках и местную секрецию цитокинов (IL–10, TGFβ). Недостаточность или дисфункции этих клеток могут вести к развитию аутоиммунных заболеваний. Эти клетки могут служить удобной мишенью при разработке новых путей индукции или отмены иммунологической толерантности к «своим» и «не своим» антигенам.</p></abstract><trans-abstract xml:lang="en"><p>Abstract. Over the past decade a population of so–called “regulatory T cells” (Treg cells) has been linked to the prevention of autoimmunity. In this review we discuss the molecular mechanisms of Treg cells development and function including the identification of the unique molecular marker of Treg cells – the transcription factor Foxp3. We discuss also the mechanisms of suppression, which include the direct cell contact through binding of cell surface molecules CTLA–4 on Treg cells to CD80/CD86 molecules of effector T cells and the local secretion of cytokines (IL–10, TGFβ). Deficiency in or dysfunction of these cells can be a cause of autoimmune disease. These cells are a good target for designing ways to induce or abrogate immunological tolerance to self and non–self antigens. (Med. Immunol., 2005, vol.7, № 4, pp. 347–354)</p></trans-abstract><kwd-group xml:lang="ru"><kwd>регуляторные Т–клетки</kwd><kwd>иммуносупрессия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>regulatory T cells</kwd><kwd>immunosuppression</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">Athanassakis I., Vassiliadis S. T–regulatory cellsare we re–discovering T suppressor? // Immunology Letters. – 2002. – Vol.84. – P.179–183.</mixed-citation><mixed-citation xml:lang="en">Athanassakis I., Vassiliadis S. T–regulatory cellsare we re–discovering T suppressor? // Immunology Letters. – 2002. – Vol.84. – P.179–183.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Bach J. 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