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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Medical academic journal</journal-id><journal-title-group><journal-title xml:lang="en">Medical academic journal</journal-title><trans-title-group xml:lang="ru"><trans-title>Медицинский академический журнал</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1608-4101</issn><issn publication-format="electronic">2687-1378</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">10064</article-id><article-id pub-id-type="doi">10.17816/MAJ1025-16</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">The role of naturally occurring regulatory CD4 +CD25 + T-cell subpopulation in the normal state and in various diseases</article-title><trans-title-group xml:lang="ru"><trans-title>Роль субпопуляции естественных регуляторных CD4 +CD25 + Т-клеток в норме и при патологии</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Akinfleva</surname><given-names>O V</given-names></name><name xml:lang="ru"><surname>Акинфиева</surname><given-names>Ольга Викторовна</given-names></name></name-alternatives><email>olgaakinf@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Bubnova</surname><given-names>L N</given-names></name><name xml:lang="ru"><surname>Бубнова</surname><given-names>Л Н</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">ФГУ «Российский научно-исследовательский институт гематологии и трансфузиологии»</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2010-06-15" publication-format="electronic"><day>15</day><month>06</month><year>2010</year></pub-date><volume>10</volume><issue>2</issue><issue-title xml:lang="en">VOL 10, NO2 (2010)</issue-title><issue-title xml:lang="ru">ТОМ 10, №2 (2010)</issue-title><fpage>5</fpage><lpage>16</lpage><history><date date-type="received" iso-8601-date="2018-09-03"><day>03</day><month>09</month><year>2018</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2010, Akinfleva O.V., Bubnova L.N.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2010, Акинфиева О.В., Бубнова Л.Н.</copyright-statement><copyright-year>2010</copyright-year><copyright-holder xml:lang="en">Akinfleva O.V., Bubnova L.N.</copyright-holder><copyright-holder xml:lang="ru">Акинфиева О.В., Бубнова Л.Н.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2013-06-15"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">http://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://journals.eco-vector.com/MAJ/article/view/10064">https://journals.eco-vector.com/MAJ/article/view/10064</self-uri><abstract xml:lang="en"><p>Naturally occurring regulatory CD4 +CD25 + T cells (Treg cells) play a crucial role in the maintenance of normal immunohomeostasis.T reg cells suppress the activity of effector T cells thus taking part in the prevention of the development of autoimmune processes, whereas the inhibition of Treg cells activity can lead to the manifestation of severe or even fatal autoimmune and lymphoproliferative diseases. It has been shown that CD4 +CD25 +Treg cells play an important role in the suppression of graft-versus-host reaction, in the prevention of the development of allergic disorders and in the suppression of immune response to opportunistic pathogens. In patients with malignant neoplasms T reg cells inhibit the productive immune response against tumor.</p></abstract><trans-abstract xml:lang="ru"><p>Естественные регуляторные CD4 +CD25 +Т-лимфоциты (Т ед-клетки) играют ключевую роль в поддержании нормального иммунного гомеостаза. Treg-клетки ингибируют активность эффекторныхТ-лимфоцитов, участвуя в предотвращении развития аутоиммунных процессов, тогда как подавление их активности может приводить к возникновению тяжелых или фатальных аутоиммунных и лимфопролиферативных заболеваний. Показана роль CD4 +CD25 +T reg-KaeTOK в супрессии реакции трансплантат против хозяина, предотвращении развития аллергических реакций, а также подавлении иммунного ответа при поражении организма патогенами. В организме пациентов со злокачественными новообразованиями Т гед-клетки подавляют противоопухолевый иммунный ответ.</p></trans-abstract><kwd-group xml:lang="en"><kwd>CD4 CD25 Treg cells</kwd><kwd>autoimmune diseases</kwd><kwd>effector T cells</kwd><kwd>allergic disorders</kwd><kwd>immune response against tumor</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>CD4 CD25 Т -клетки</kwd><kwd>аутоиммунные заболевания</kwd><kwd>эффекторные Т-лимфоциты</kwd><kwd>аллергические реакции</kwd><kwd>противоопухолевый иммунный ответ</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Быковская С.Н., Насонов Е.Л. Роль дефектов иммуносупрессии в развитии аутоиммунных заболеваний // Науч. практ. ревматол. 2005. № 4. С. 81-84.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Воробьев А.А., Быковская С.Н., Пашков Е.П. и др. Роль клеток-регуляторов CD25+CD4+ в развитии хронических инфекционных заболеваний // Вести. 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