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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="other" dtd-version="1.2" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">Russian Journal of Allergy</journal-id><journal-title-group><journal-title xml:lang="en">Russian Journal of Allergy</journal-title><trans-title-group xml:lang="ru"><trans-title>Российский Аллергологический Журнал</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1810-8830</issn><issn publication-format="electronic">2686-682X</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">17141</article-id><article-id pub-id-type="doi">10.36691/RJA17141</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Original study articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Оригинальные исследования</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">IMMUNOPATHOGENETIC AND CLINICAL ASPECTS OF ANTIBODY FORMATION TO CATALASE IN SYSTEMIC LUPUS ERYTHEMATOSUS</article-title><trans-title-group xml:lang="ru"><trans-title>ИММУНОПАТОГЕНЕТИЧЕСКИЕ И КЛИНИЧЕСКИЕ АСПЕКТЫ АНТИТЕЛООБРАЗОВАНИЯ К КАТАЛАЗЕ ПРИ СИСТЕМНОЙ КРАСНОЙ ВОЛЧАНКЕ</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3951-8985</contrib-id><name-alternatives><name xml:lang="en"><surname>Emelyanova</surname><given-names>Olga</given-names></name><name xml:lang="ru"><surname>Емельянова</surname><given-names>Ольга Ивановна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>Cand.med. Sci, Leading research fellow</p></bio><bio xml:lang="ru"><p>ведущий научный сотрудник</p></bio><email>emelyanova.vlg@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1627-8483</contrib-id><contrib-id contrib-id-type="spin">4890-3630</contrib-id><name-alternatives><name xml:lang="en"><surname>Trofimenko</surname><given-names>Andrey Stepanovich</given-names></name><name xml:lang="ru"><surname>Трофименко</surname><given-names>Андрей Степанович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>зав. лаб клинико-иммунологической лаб.</p></bio><email>a.s.trofimenko@mail.ru</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7080-2442</contrib-id><contrib-id contrib-id-type="spin">6918-8380</contrib-id><name-alternatives><name xml:lang="en"><surname>Rusanova</surname><given-names>Olga Aleksandrovna</given-names></name><name xml:lang="ru"><surname>Русанова</surname><given-names>Ольга Александровна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>младший научный сотрудник</p></bio><email>rusanova28@rambler.ru</email><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Ivanovna</surname><given-names>CHernova Svetlana</given-names></name><name xml:lang="ru"><surname>Ивановна</surname><given-names>Чернова Светлана</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>director of the institute</p></bio><bio xml:lang="ru"><p>директор института</p></bio><email>sichernova@yandex.ru</email><xref ref-type="aff" rid="aff3"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">FSBI Research Institute for Clinical and Experimental Rheumatology named after A.B.Zborovsky</institution></aff><aff><institution xml:lang="ru">ФГБНУ "Научно-исследовательский институт клинической и экспериментальной ревматологии имени А.Б.Зборовского"</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Federal State Budgetaty Institution @Research Institute of Clinical and Experimental rheumatology named after A.B.Zborovsky</institution></aff><aff><institution xml:lang="ru">ФГБНУ "НИИ КиЭР им. А.Б.Зборовского</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="en">Clinical and Federal State Budgetaty Institution @Research Institute of Experimental Rheumatology named after A.B.Zborovsky</institution></aff><aff><institution xml:lang="ru">ФГБНУ "НИИ КиЭР им. А.Б.Зборовского"</institution></aff></aff-alternatives><content-language>ru</content-language><pub-date date-type="preprint" publication-format="electronic" iso-8601-date="2026-09-21"><day>21</day><month>09</month><year>2026</year></pub-date><volume>23</volume><issue>4</issue><issue-title xml:lang="ru"/><history><date date-type="received" iso-8601-date="2026-07-09"><day>09</day><month>07</month><year>2026</year></date><date date-type="accepted" iso-8601-date="2026-09-14"><day>14</day><month>09</month><year>2026</year></date></history><pub-history><event event-type="received"><event-desc>Received:<date date-type="received" iso-8601-date="2026-07-09"><day>09</day><month>07</month><year>2026</year></date></event-desc></event><event event-type="accepted"><event-desc>Accepted:<date date-type="accepted" iso-8601-date="2026-09-14"><day>14</day><month>09</month><year>2026</year></date></event-desc></event></pub-history><permissions><copyright-statement xml:lang="en">Copyright ©; , ABV-press</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; , АБВ-пресс</copyright-statement><copyright-holder xml:lang="en">ABV-press</copyright-holder><copyright-holder xml:lang="ru">АБВ-пресс</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2028-09-21"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://rusalljournal.ru/raj/about/submissions#copyrightNotice</ali:license_ref></license></permissions><self-uri xlink:href="https://rusalljournal.ru/raj/article/view/17141">https://rusalljournal.ru/raj/article/view/17141</self-uri><abstract xml:lang="en"><p><bold>Objective.</bold><bold> </bold>Study of the clinical and pathogenetic role of anti-catalase antibodies in systemic lupus erythematosus (SLE) using a technology involving antigen immobilization on magnetic polyacrylamide beads. <bold>Materials and methods</bold><bold>.</bold> The study included 56 patients with SLE aged over 18 years who were receiving inpatient treatment in rheumatology department; the diagnosis of SLE was verified according to the 2019 EULAR/ACR criteria. SLE disease activity was assessed using the SLEDAI-2K scale. The SLICC/ACR DI index was used to quantify accumulated organ damage. The control group consisted of 30 apparently healthy individuals. Catalase activity in blood serum was measured spectrophotometrically using ammonium molybdate. The level of IgG antibodies against catalase (AKA) in blood serum was determined using an enzyme-linked immunosorbent assay (ELISA) in a proprietary modification. <bold>Results</bold>. It has been established that catalase activity levels in patients with SLE were significantly lower than in healthy individuals. An inverse correlation was found between enzyme activity and ACA levels in patients with this disease. It was shown that the highest ACA levels are observed in cases of SLE with high disease activity. ACA concentrations upon hospital admission differed significantly between SLE patients with skin or CNS involvement and those without such involvement. To study biomarker dynamics during treatment, the SLE group was divided into two subgroups: patients who underwent intensification of immunosuppressive therapy during hospitalization (66.1%) and patients on a stable treatment regimen (33.9%). The mean change in SLE disease activity in the dose-escalation subgroup was -5.05 ± 0.72 SLEDAI-2K points, whereas in the stable-therapy subgroup, it was -0.14 ± 0.33 SLEDAI-2K points. In the dose-escalation subgroup, a statistically significant inverse correlation was observed between the change in SLE disease activity and the change in catalase activity, as well as a weaker positive correlation between the former parameter and the change in ACA concentration.<bold>Conclusion</bold>. Our findings indicate a significant role for catalase in the pathogenesis of SLE and point to the potential for developing innovative biomarkers—based on catalase and ACA activity—that reflect the efficacy of therapy for this disease.</p></abstract><trans-abstract xml:lang="ru"><p><bold>Цель исследования: </bold>Изучение клинической и патогенетической роли антител к каталазе при системной красной волчанке (СКВ) с использованием технологии иммобилизации антигена на полиакриламидных гранулах с магнитными свойствами.</p> <p><bold>Методы:</bold> В исследование было включено 56 больных СКВ старше 18 лет, находившихся на стационарном лечении в ревматологическом отделении, диагноз СКВ верифицировали согласно критериям EULAR/ACR 2019 г. Уровень активности СКВ оценивали по шкале SLEDAI-2K. Для количественной оценки накопленного повреждения организма использовали индекс SLICC/ACR DI. Контрольную группу составили 30 практически здоровых лиц. Активность каталазы в сыворотке крови измеряли спектрофотометрическим методом с использованием молибдата аммония. Определение уровня антител к каталазе класса IgG (АКА) в сыворотке крови проводили методом иммуноферментного анализа в оригинальной модификации.</p> <p><bold>Результаты: </bold>Установлено, что у пациентов с СКВ уровень активности каталазы был значимо ниже, чем у здоровых лиц. Выявлена обратная корреляция между активностью фермента и АКА у больных данным заболеванием. Показано, что наиболее высокие уровни АКА обнаруживаются при СКВ с высокой активностью болезни. Концентрация АКА при поступлении в стационар существенно различалась у пациентов с СКВ, имеющих поражение кожи или ЦНС, и у больных без таких поражений. Для изучения динамики биомаркеров в ходе лечения группа СКВ была разделена на 2 подгруппы: больные, которым во время госпитализации производилась интенсификация иммуносупрессивной терапии (66,1%), и пациенты со стабильной схемой лечения (33,9%). Средняя динамика активности СКВ в подгруппе эскалации составила -5,05±0,72 балла SLEDAI-2K, в подгруппе стабильной терапии — -0,14±0,33 балла SLEDAI-2K. В подгруппе эскалации наблюдалась статистически значимая обратная корреляция между динамикой активности СКВ и динамикой активности каталазы, а также прямая корреляция меньшей силы — между первым показателем и динамикой концентрации АКА.</p> <p><bold>Заключение</bold>: Полученные нами результаты свидетельствуют о значимой роли каталазы в патогенезе СКВ и о возможности разработки инновационных биомаркеров, отражающих эффективность терапии данного заболевания, с использованием активности каталазы и АКА.</p></trans-abstract><kwd-group xml:lang="en"><kwd>Key words: catalase, systemic lupus erythematosus, diagnosis, magnetic sorbents, antibodies, activity.</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>Ключевые слова: каталаза, системная красная волчанка, антитела, магнитосорбенты</kwd></kwd-group><funding-group><funding-statement xml:lang="en">The study received no sponsorship support</funding-statement><funding-statement xml:lang="ru">Исследование не имело спонсорской поддержки.</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">м1.	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