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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">10.14412/1995-4484-2017-245-251</article-id><article-id custom-type="elpub" pub-id-type="custom">rsp-2376</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 RESEARCH</subject></subj-group></article-categories><title-group><article-title>Взаимосвязь FoxP3+ регуляторных Т-клеток с активностью заболевания и уровнем антител при раннем ревматоидном артрите</article-title><trans-title-group xml:lang="en"><trans-title>THE RELATIONSHIP OF FoxP3+ T REGULATORY CELLS TO DISEASE ACTIVITY AND ANTIBODY LEVELS IN EARLY RHEUMATOID ARTHRITIS</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>Авдеева</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Avdeeva</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522 Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><email xlink:type="simple">9056249400@mail.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>Рубцов</surname><given-names>Ю. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Rubtsov</surname><given-names>Yu. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кафедра биохимии и молекулярной медицины факультета фундаментальной медицины</p><p>119192 Москва, Ломоносовский проспект, 31, корп. 5</p></bio><bio xml:lang="en"><p>Department of Biochemistry and Molecular Medicine, Faculty of Fundamental Medicine</p><p>31, Lomonosovsky Prospect, Build. 5, Moscow 119192</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Дыйканов</surname><given-names>Д. Т.</given-names></name><name name-style="western" xml:lang="en"><surname>Dyikanov</surname><given-names>D. T.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кафедра биохимии и молекулярной медицины факультета фундаментальной медицины</p><p>119192 Москва, Ломоносовский проспект, 31, корп. 5</p></bio><bio xml:lang="en"><p>Department of Biochemistry and Molecular Medicine, Faculty of Fundamental Medicine</p><p>31, Lomonosovsky Prospect, Build. 5, Moscow 119192</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Попкова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Popkova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><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-1"/></contrib><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>кафедра ревматологии Института профессионального образования</p><p>115522 Москва, Каширское шоссе, 34А</p><p>119991 Москва, ул. Трубецкая, 8, стр. 2 </p></bio><bio xml:lang="en"><p>Department of Rheumatology, Institute of Professional Education</p><p>34A, Kashirskoe Shosse, Moscow 115522</p><p>8, Trubetskaya St., Build. 2, Moscow 119991 </p></bio><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», Москва<country>Россия</country></aff><aff xml:lang="en">V.A. Nasonova Research Institute of Rheumatology, Moscow<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова»<country>Россия</country></aff><aff xml:lang="en">M.V. Lomonosov Moscow State University<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru">ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», Москва;  &#13;
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России<country>Россия</country></aff><aff xml:lang="en">V.A. Nasonova Research Institute of Rheumatology, Moscow; &#13;
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>09</day><month>07</month><year>2017</year></pub-date><volume>55</volume><issue>3</issue><fpage>245</fpage><lpage>251</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Авдеева А.С., Рубцов Ю.П., Дыйканов Д.Т., Попкова Т.В., Насонов Е.Л., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Авдеева А.С., Рубцов Ю.П., Дыйканов Д.Т., Попкова Т.В., Насонов Е.Л.</copyright-holder><copyright-holder xml:lang="en">Avdeeva A.S., Rubtsov Y.P., Dyikanov D.T., Popkova T.V., Nasonov E.L.</copyright-holder><license 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/2376">https://rsp.mediar-press.net/rsp/article/view/2376</self-uri><abstract><p>Цель – проанализировать взаимосвязь количества FoxP3+ регуляторных Т-клеток (Трег) с клинико-лабораторными показателями активности заболевания и уровнем антител в группе пациентов с ранним ревматоидным артритом (РА).</p><sec><title>Материал и методы</title><p>Материал и методы. В исследование были включены 45 не получавших ранее терапии метотрексатом пациентов с ранним РА (критерии ACR/EULAR 2010 г.), в том числе 39 женщин; медиана возраста составила 52,0 [32,5; 57,5] года, длительность заболевания – 5 [4; 6] мес, DAS28 – 5,01 [4,18; 5,8]; 71,1% больных были позитивны по ревматоидному фактору (РФ) и 88,9% позитивны по антителам к циклическому цитруллинированному пептиду (АЦЦП). Относительное и абсолютное количество Трег (FoxP3+CD25+; CD152+surface; CD152+intracellular; FoxP3+CD127-; CD25+CD127-; FoxP3+ICOS+; FoxP3+CD154+; FoxP3+CD274+) определялось методом иммунофлюоресцентного окрашивания и многоцветной проточной цитофлюориметрии. Контрольную группу составили 20 здоровых доноров, сопоставимых по полу и возрасту с обследованными больными.</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. У 22 (48,9%) больных была высокая, у 20 (44,4%) – умеренная и у 3 (6,7%) – низкая активность патологического процесса по DАS28. У пациентов с ранним РА, по сравнению со здоровыми донорами, отмечалось более низкое процентное количество (ПК) FoxP3+CD25+ клеток, ПК и абсолютное содержание (абс.) FoxP3+ICOS+ клеток, ПК и абс. FoxP3+CD154+ и FoxP3+ CD274+ Т-клеток; p&lt;0,05 во всех случаях. Регистрировалась отрицательная корреляционная взаимосвязь: ПК FoxP3+CD25+ с С-реактивным белком (СРБ) (r=-0,4); ПК CD152+intracellular с DAS28 (r=-0,35), СОЭ (r=-0,46), СРБ (r=-0,54); ПК FoxP3+CD127- с СРБ (r= -0,42); ПК CD25+CD127- с DAS28 (r=-0,38), SDAI (r=-0,41), CDAI (r=-0,36), СОЭ (r=-0,39), СРБ (r=-0,47); р&lt;0,05 во всех случаях.</p><p>Среди серонегативных по РФ больных была выявлена более высокая ПК CD25+CD127-, ПК и абс. Foxp3+CD154+ и Foxp3+CD274+ Т-лимфоцитов.</p></sec><sec><title>Заключение</title><p>Заключение. Представленные данные позволяют говорить о снижении количества и функциональной активности Трег при раннем РА, что ассоциируется с более высокой активностью заболевания, наличием системных проявлений болезни, а также сопровождается гиперпродукцией антител.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Objective</title><p>Objective: to analyze the relationship of the count of FoxP3+ T regulatory cells (Tregs) to the clinical and laboratory parameters of disease activity and the levels of antibodies in a group of patients with early rheumatoid arthritis (RA).</p></sec><sec><title>Subjects and methods</title><p>Subjects and methods. The investigation enrolled 45 patients with early RA (2010 ACR/EULAR criteria) who had not previously received treatment with methotrexate, including 39 women; median age was 52.0 [32.5; 57.5] years; disease duration, 5 [4; 6] months, DAS28 5.01 [4.18; 5.8]; 71.1% of the patients were rheumatoid factor (RF) positive and 88.9% were anti-cyclic citrullinated peptide positive. The relative and absolute counts of Treg (FoxP3+CD25+; CD152+surface; CD152+intracellular; FoxP3+CD127-; CD25+CD127-; FoxP3+ICOS+; FoxP3+CD154+; FoxP3+CD274+) were measured by immunofluorescence staining and multicolor flow cytometry. A control group consisted of 20 healthy donors who were matched for sex and age with the examined patients.</p></sec><sec><title>Results and discussion</title><p>Results and discussion. DАS28 was high, moderate, and low in 22 (48.9%), 20 (44.4%), and 3 (6.7%) patients, respectively. As compared with the healthy donors, the patients with early RA were observed to have lower values in the percentage of FoxP3+CD25+ cells, in the percentage and absolute count of FoxP3+ICOS+ cells, in the percentage and absolute count of FoxP3+CD154+ and FoxP3+ CD274+ T cells; p&lt;0.05 in all cases. Negative correlation was recorded between the percentage of FoxP3+CD25+ and C-reactive protein (CRP) (r=-0.4); that of CD152+intracellular and DAS28 (r=-0.35), ESR (r=-0.46), CRP (r=-0.54); that of FoxP3+CD127 and CRP (r=-0.42); that of CD25+CD127 and DAS28 (r=-0.38), SDAI (r=-0.41), CDAI (r=-0.36), ESR (r=-0.39), CRP (r=-0.47); p&lt;0.05 in all cases.</p><p>The patients who were seronegative for RF were found to have higher values in the percentage of CD25+CD127, in the percentage and absolute count of Foxp3+CD154+ and Foxp3+CD274+ T lymphocytes.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>ранний ревматоидный артрит</kwd><kwd>активность заболевания</kwd><kwd>аутоантитела</kwd><kwd>регуляторные Т-лимфоциты</kwd></kwd-group><kwd-group xml:lang="en"><kwd>early rheumatoid arthritis</kwd><kwd>disease activity</kwd><kwd>autoantibodies</kwd><kwd>T regulatory lymphocytes</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">Быковская СН, Насонов ЕЛ. 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