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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-ROC-16676</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-3045</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>КРАТКИЕ СООБЩЕНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SHORT COMMUNICATIONS</subject></subj-group></article-categories><title-group><article-title>Роль CD20+Т-лимфоцитов в патогенезе рассеянного склероза</article-title><trans-title-group xml:lang="en"><trans-title>Role of CD20+T lymphocytes in the pathogenesis of multiple sclerosis</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>Глебездина</surname><given-names>Н. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Glebezdina</surname><given-names>N. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Глебездина Наталья Сергеевна - к.б.н., младший научный сотрудник лаборатории иммунорегуляции,</p><p>614081, г. Пермь, ул. Голева, 13</p></bio><bio xml:lang="en"><p>Natalia S. Glebezdina - PhD (Biology), Junior Research Associate, Laboratory of Immunoregulation,</p><p>13 Golev St, Perm 614081</p><p> </p></bio><email xlink:type="simple">glebezdina_n@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Институт экологии и генетики микроорганизмов Уральского отделения Российской академии наук – филиал ФГБУН «Пермский федеральный исследовательский центр Уральского отделения Российской академии наук»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Ecology and Genetics of Microorganisms, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>26</day><month>07</month><year>2024</year></pub-date><volume>26</volume><issue>4</issue><fpage>749</fpage><lpage>754</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Глебездина Н.С., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Глебездина Н.С.</copyright-holder><copyright-holder xml:lang="en">Glebezdina N.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/3045">https://www.mimmun.ru/mimmun/article/view/3045</self-uri><abstract><p>CD3+CD20+Т-лимфоциты представляют собой популяцию клеток, которая наряду со стандартными Т-клеточными маркерами экспрессирует нетипичную мембранную молекулу CD20 (традиционный В-клеточный маркер). Эти клетки идентифицированы не так давно и в настоящий момент активно изучаются. В норме они составляют до 3-5% компартмента CD3+T-клеток в периферической крови человека, а также обнаружены в первичных и вторичных лимфоидных органах, в спинномозговой жидкости, тканях головного мозга и печени. У здоровых людей CD3+CD20+Тклетки гетерогенны и содержат меньшую долю CD4+ клеток, но продуцируют более высокие уровни GM-CSF, IFNγ, IL-17, TNFα, IL-4, IL-10, молекул адгезии и хемокиновых рецепторов, чем CD3+CD20-Т-клетки, что указывает на высокоактивированный провоспалительный фенотип со свойствами, потенциально способствующими их патогенной инфильтрации в ЦНС. Недавними исследованиями установлено патогенное поведение CD3+CD20+Т-клеток при широком спектре заболеваний, включая гематологические и негематологические CD20+Т-клеточные злокачественные новообразования и ВИЧ, а также аутоиммунные патологии, в частности рассеянный склероз – инвалидизирующее воспалительное нейродегенеративное заболевание, которое сопровождается поражением миелиновой оболочки нервных волокон. CD20-позитивные Т-клетки выявляются у больных рассеянным склерозом в периферической крови, спинномозговой жидкости (встречаются с частотой, сходной с частотой В-клеток, и демонстрируют корреляцию с тяжестью заболевания) и белом веществе головного мозга. Показано, что CD20-позитивные Т-лимфоциты в периферической крови пациентов с рассеянным склерозом продуцируют высокие уровни IFNγ и IL-17А, которые являются двумя провоспалительными цитокинами, участвующими в патогенезе этого заболевания. Возможно, что CD20+Т-клетки представляют собой отдельную субпопуляцию клеток Th17, так называемых Th1-поляризованных Th17, которые являются продуктом редифференцировки клеток Th17 в Th1 и сочетают фенотипические характеристики обеих популяций. И экспрессия CD20 может являться потенциальным маркером, определяющим целевую субпопуляцию таких патогенных Т-клеток, а также служить мишенью для терапии аутоиммунных заболеваний.</p></abstract><trans-abstract xml:lang="en"><p>CD3+CD20+T lymphocytes are a population of T cells that, along with standard T cell markers, express the atypical membrane molecule CD20 (a traditional B cell marker). These cells were identified not so long ago and are currently being actively studied. Normally, they constitute up to 3-5% of the CD3+T cell compartment in human peripheral blood, and are also found in primary and secondary lymphoid organs, cerebrospinal fluid, brain tissue and liver. In healthy individuals, CD3+CD20+T cells are heterogeneous and contain a lower proportion of CD4+ cells, but produce higher levels of GM-CSF, IFNγ, IL-17, TNFα, IL-4, IL-10, adhesion molecules and chemokine receptors than CD3+CD20-T cells, indicating a highly activated proinflammatory phenotype with properties potentially promoting their pathogenic infiltration into the CNS. Recent studies have established the pathogenic behavior of CD3+CD20+T cells in a wide range of diseases, including hematological and non-hematological CD20+T cell malignancies and HIV, as well as autoimmune pathologies, in particular multiple sclerosis, a disabling inflammatory neurodegenerative disease that is accompanied by damage to the myelin sheath nerve fibers. CD20 positive T cells are detected in patients with multiple sclerosis in the peripheral blood, cerebrospinal fluid (occur at a frequency similar to that of B cells and show a correlation with disease severity) and white matter of the brain. CD20 positive T lymphocytes in the peripheral blood of patients with multiple sclerosis have been shown to produce high levels of IFNγ and IL-17А, which are two proinflammatory cytokines involved in the pathogenesis of this disease. It is possible that CD20+T cells represent a separate subpopulation of Th17 cells, the so-called Th1-polarized Th17, which are the product of redifferentiation of Th17 cells into Th1 and combine the phenotypic characteristics of both populations. And the expression of CD20 T cells may be a valuable marker that determines the target subpopulation of such pathogenic T cells, as well as serve as a target for therapy of autoimmune diseases.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>CD20+Т-лимфоциты</kwd><kwd>Th1</kwd><kwd>Th17</kwd><kwd>Th1-поляризованные Th17</kwd><kwd>IFNγ</kwd><kwd>IL-17А</kwd><kwd>аутоиммунные заболевания</kwd><kwd>рассеянный склероз</kwd></kwd-group><kwd-group xml:lang="en"><kwd>CD20+T lymphocytes</kwd><kwd>Th1</kwd><kwd>Th17</kwd><kwd>Th1-polarized Th17</kwd><kwd>IFNγ</kwd><kwd>IL-17А</kwd><kwd>autoimmune diseases</kwd><kwd>multiple sclerosis</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена в рамках государственного задания, номер госрегистрации темы: 124020500027-7.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Куклина Е.М., Глебездина Н.С. 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