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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">tumors</journal-id><journal-title-group><journal-title xml:lang="ru">Malignant tumours</journal-title><trans-title-group xml:lang="en"><trans-title>Malignant tumours</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2224-5057</issn><issn pub-type="epub">2587-6813</issn><publisher><publisher-name>Rosoncoweb</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18027/2224-5057-2015-1-24-30</article-id><article-id custom-type="elpub" pub-id-type="custom">tumors-35</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>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL REPORTS</subject></subj-group></article-categories><title-group><article-title>НОВЫЕ ВОЗМОЖНОСТИ РЕГУЛЯЦИИ ПРОТИВООПУХОЛЕВОГО ИММУННОГО ОТВЕТА</article-title><trans-title-group xml:lang="en"><trans-title>New capabilities of regulation of antitumor immune response</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>КАДАГИДЗЕ</surname><given-names>З. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Kadagidze</surname><given-names>Z. G.</given-names></name></name-alternatives><email xlink:type="simple">kad-zaira@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>ЧЕРТКОВА</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Chertkova</surname><given-names>A. I.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>ЗАБОТИНА</surname><given-names>Т. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Zabotina</surname><given-names>T. N.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>КОРОТКОВА</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Korotkova</surname><given-names>O. V.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>СЛАВИНА</surname><given-names>Е. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Slavina</surname><given-names>E. G.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>БОРУНОВА</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Borunova</surname><given-names>A. A.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>НИИ клинической онкологии ФГБУ «РОНЦ им. Н. Н. Блохина»</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>20</day><month>05</month><year>2015</year></pub-date><volume>0</volume><issue>1</issue><fpage>26</fpage><lpage>34</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; КАДАГИДЗЕ З.Г., ЧЕРТКОВА А.И., ЗАБОТИНА Т.Н., КОРОТКОВА О.В., СЛАВИНА Е.Г., БОРУНОВА А.А., 2015</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="ru">КАДАГИДЗЕ З.Г., ЧЕРТКОВА А.И., ЗАБОТИНА Т.Н., КОРОТКОВА О.В., СЛАВИНА Е.Г., БОРУНОВА А.А.</copyright-holder><copyright-holder xml:lang="en">Kadagidze Z.G., Chertkova A.I., Zabotina T.N., Korotkova O.V., Slavina E.G., Borunova A.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://www.malignanttumors.org/jour/article/view/35">https://www.malignanttumors.org/jour/article/view/35</self-uri><abstract><p>Опухоль обладает различными механизмами, способными разрушать иммунологическую защиту. Популяции регуляторных клеток наряду с другими факторами обеспечивают «ускользание» опухоли от иммунологического надзора. В нашей лаборатории было проведено изучение особенностей количественных изменений некоторых субпопуляций лимфоцитов периферической крови у первично-операбельных больных раком молочной железы (РМЖ) и диссеминированной меланомой на разных этапах опухолевого роста и в процессе противоопухолевой терапии. У 94,5% больных РМЖ было обнаружено повышение по сравнению с контролем количества NKT-клеток с фенотипом CD45+CD3+CD16+CD56+, у 78% повышение количества CD8+CD28- Т-клеток, и у 20,5% больных повышение количества регуляторных CD4+CD25+FOXP3+ Т-клеток. Выявлена зависимость изменений количества этих клеток от стадии заболевания: у пациенток с I и II стадиями заболевания отмечалось статистически значимое повышение процента CD8+CD28- Т-клеток и CD45+CD3+CD16+CD56+ NKT-клеток по сравнению с донорами. В то же время у пациенток с III стадией количество клеток обеих популяций снижалось и практически не отличалось от нормы. Подобная динамика количественных изменений была характерна и для основных популяций клеток-эффекторов противоопухолевого иммунитета. При обследовании больных диссеминированной меланомой было обнаружено, что отсутствие повышения количества цитотоксических CD45+CD8+CD11b+ Т-клеток в процессе лечения дендритноклеточной вакциной (ДКВ), по-видимому, является показанием к прекращению вакцинотерапии, а исходно повышенное количество CD3+CD8+CD16+ NKT-клеток может служить основанием для отказа от ДКВ. Приводится краткое описание основных ко-ингибиторных рецепторов Т-клеток и моноклональных антител, блокирующих ингибиторные молекулы на иммунокомпетентных и опухолевых клетках, с целью повышения эффективности противоопухолевого иммунного ответа. Обнадеживающие клинические результаты были получены при применении анти-CTLA-4 (ипилимумаб) и анти-PD-1 (ниволумаб) моноклональных антител.</p></abstract><trans-abstract xml:lang="en"><p>The tumor has different mechanisms capable of destroying the immunological protection. Population of regulatory cells, along with other factors provide “escape” of the tumor from immune surveillance. In our laboratory, we studied the features of quantitative changes of some subpopulations of peripheral blood lymphocytes in primary operable breast cancer (BC) and melanoma at different stages of tumor growth and in the process of tumor therapy. In 94.5% of patients with breast cancer were found to increase compared to the control amount of NKT-cells with the phenotype CD45+CD3+ CD16+CD56+, 78% increase in number of CD8+CD28– T-cells, and 20.5% increase in the number of patients Regulatory CD4+CD25+FOXP3+ T cells. Was found to depend on changes in the number of these cells from the stage of the disease. Patients with stage I and II disease there was a statistically significant increase in the percentage of CD8+CD28– T–cells and CD45+CD3+ CD16+CD56+ NKT-cells compared to the donor. At the same time in patients with stage III the number of cells of both populations declined and did not differ from the norm. Such dynamics of quantitative changes were typical for the main populations of effector cells antitumor immunity. In the evaluation of patients with disseminated melanoma was found that no increase in the number of cytotoxic CD45+CD8+CD11b+ T cells in the treatment dendritic cell vaccine (DCV) appears to be an indication to stop vaccine therapy, initially increased amount of CD3+CD8+CD16+. NKT-cells may serve as grounds for refusal of DCV. A brief description of the major co-receptor inhibitor of T-cells, and monoclonal antibodies that block the inhibitory molecule on immune and tumor cells in order to increase the efficiency of anti-tumor immune response. Encouraging clinical results have been obtained by using anti-CTLA-4 (ipilimumab), and anti-PD-1 (nivolumab) monoclonal antibodies.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>регуляторные Т-клетки</kwd><kwd>NKT-клетки</kwd><kwd>меланома</kwd><kwd>рак молочной железы</kwd><kwd>ко-ингибиторные и ко-стимуляторные рецепторы Т-клеток</kwd><kwd>таргетная терапия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>regulatory T-cells</kwd><kwd>NKT-cells</kwd><kwd>melanoma</kwd><kwd>breast cancer</kwd><kwd>co-inhibitory and co-stimulatory receptors of T cell</kwd><kwd>targeted therapy</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">Кадагидзе З. Г., Черткова А. И., Славина Е. Г. NKT клетки и противоопухолевый иммунитет. // РБЖ — 2011. — Том. 10, № 3 — Стр. 9. —15.</mixed-citation><mixed-citation xml:lang="en">Kadagidze Z.G., Chertkova A.I., Slavina E.G. 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