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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-IFO-3026</article-id><article-id custom-type="elpub" pub-id-type="custom">mimmun-3026</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>Иммунологические особенности различных фенотипов хронического риносинусита</article-title><trans-title-group xml:lang="en"><trans-title>Immunological features of different phenotypes in chronic rhinosinusitis</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>Лазарева</surname><given-names>А. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Lazareva</surname><given-names>A. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Лазарева А.М. – к.м.н., младший научный сотрудник </p><p>660022, г. Красноярск, ул. Партизана Железняка, 3г</p></bio><bio xml:lang="en"><p>Lazareva A.M., PhD (Medicine), Junior Research Associate </p><p>3g Partizan Zheleznyak St, Krasnoyarsk, 660022</p></bio><email xlink:type="simple">a.m.lazareva88@gmail.com</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>Смирнова</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Smirnova</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Смирнова О.В. – д.м.н., профессор, заведующая лабораторией молекулярно-клеточной патофизиологии </p><p>660022, г. Красноярск, ул. Партизана Железняка, 3г</p></bio><bio xml:lang="en"><p>Smirnova O.V., PhD, MD (Medicine), Professor, Head, Laboratory of Molecular Cellular Pathophysiology </p><p>3g Partizan Zheleznyak St, Krasnoyarsk, 660022</p></bio><email xlink:type="simple">ovsmirnova71@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт медицинских проблем Севера»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Research Institute of Medical Problems of the North</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>14</day><month>10</month><year>2024</year></pub-date><volume>27</volume><issue>2</issue><fpage>275</fpage><lpage>286</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Лазарева А.М., Смирнова О.В., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Лазарева А.М., Смирнова О.В.</copyright-holder><copyright-holder xml:lang="en">Lazareva A.M., Smirnova O.V.</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/3026">https://www.mimmun.ru/mimmun/article/view/3026</self-uri><abstract><p>Хронический риносинусит (ХРС) – патология, которая проявляется воспалением в верхних дыхательных путях и в которой можно выделить два главных фенотипа: РС с полипозной тканью в носу и околоносовых пазухах и РС без полипов. Полагаясь на высокие концентрация различных цитокинов, воспалительные реакции при ХРС можно разделить на три эндотипа: Тh1 (IFNγ), Th2 (IL-4, IL-5 и IL-13) и Тh3 (IL-17, IL-22). Патогенез воспаления как при ХРС без назальных полипов, так и при ХРС с назальными полипами достаточно различен, а частота встречаемости вышеуказанных эндотипов весьма противоречива по данным исследований, что подтверждает целесообразность дальнейшего изучения этапов развития ХРС. Эти важные медико-социальные черты заболеваний слизистой носа и придаточных пазух обуславливают необходимость дальнейшего исследования патогенеза ХРС. В данном обзоре освещена информация об иммунологических особенностях и дисфункциях, приводящих к появлению хронического риносинусита с полипами или без них. Цель данного обзора – изучить по данным литературы влияние первой линии защиты компонентов врожденного и приобретенного иммунитета на патогенез полипозного и неполипозного ХРС. В статье представлен обзор зарубежной научной литературы. Авторами был проведен научный поиск по тематике иммунного ответа при формировании хронических риносинуситов с полипами и без них. Использовали соответствующие ключевые слова и фильтры в поисковых системах PubMed и Google Scholar, по базам данных Scopus, Web of Science. Низкая эффективность различных используемых методов лечения может быть обусловлена гетерогенной иммунопатологией. Использование биологических препаратов, хотя и одобрено, может быть ненадежным, поскольку эти препараты, воздействующие на Тh2, могут вводиться пациентам с заболеванием, не связанным с Тh2. Наличие эозинофилов и гноя могут дать основу для экстраполяции эндотипа, но сейчас у врачей, лечащих ХРС, нет широкого распространенного доступа к лабораторным анализам для типирования РС и обоснования медикаментозной тактики. Пациенты с любым типом воспаления могут страдать от скрытых инфекций, вызванных бактериями и грибами или вирусами, и это затрудняет диагностику поляризации иммунного ответа. Дальнейшее изучение звеньев иммунологического патогенеза ХРС позволит разработать персонифицированный алгоритм диагностики и лечения таких больных.</p></abstract><trans-abstract xml:lang="en"><p>Chronic rhinosinusitis (CRS) is a disease which manifests with inflammation of the upper respiratory tract. Two main phenotypes can be distinguished in CRS: a clinical form with polypous tissue, and a clinical variant without polyposis. With regard of increased cytokine concentrations, the inflammatory response in CRS can be divided into 3 endotypes: Th1 (IFNγ), Th2 (IL-4, IL-5, IL-13) and Th3 type (IL-17, IL-22). The pathogenesis of inflammation in CRS with nasal polyps and polyposis-free cases is quite different, and, according to current publications, the data on prevalence of different endotypes is very contradictory, thus confirming the need for further studies of CRS development. These important medical and social features of diseases affecting nasal mucosa and paranasal sinuses require further studies in pathogenesis of CRS. This review covers information about the immunological features and dysfunctions that lead to occurence of CRS with or without polyps. The purpose of this review article is to study the influence of the first-line immune defense, components of innate and acquired immunity on the pathogenesis of CRS.The article provides a review of the worldwide research publications in the field. The authors conducted a search for different items of immune response related to development of CRS with and without polyps. We used keywords and filters in the PubMed and Google Scholar, as well as in Scopus and Web of Science databases. So far, low efficiency of various treatment methods used may be due to heterogeneous immunopathology. The use of biological preparations, although approved, may be non-reliable, since these Th2-targeted drugs may be administered to patients with non-Th2 disease. The presence of eosinophils and pus may provide a basis for endotype extrapolation. However, the clinicians treating CRS do not have widespread access to laboratory tests in order to specify the CRS type and to administer a tailored drug management. Patients with any type of inflammation may suffer from latent infections caused by bacteria, fungi or viruses, thus making difficult a specific evaluation of polarized immune response. Further studies on the links of immunological pathogenesis in CRS will allow us to develop a personalized algorithm for the diagnosis and treatment of such patients.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хронический риносинусит</kwd><kwd>полипозный риносинусит</kwd><kwd>эндотипы</kwd><kwd>иммунный ответ</kwd><kwd>патогенез</kwd><kwd>фенотип</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic rhinosinusitis</kwd><kwd>polypous rhinosinusitis</kwd><kwd>endotypes</kwd><kwd>immune response</kwd><kwd>pathogenesis</kwd><kwd>phenotype</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">Bae C.H., Na H.G., Choi Y.S., Song S.Y., Kim Y.D. Clusterin induces MUC5AC expression via activation of NF-kappaB in human airway epithelial cells. Clin. Exp. 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