Annals of the Russian academy of medical sciencesAnnals of the Russian academy of medical sciencesВестник Российской академии медицинских наук0869-60472414-3545"Paediatrician" Publishers LLC1819410.15690/vramn18194IMMUNOLOGY: CURRENT ISSUESАКТУАЛЬНЫЕ ВОПРОСЫ ИММУНОЛОГИИReview ArticleAssessing the role of interferons in congenital and acquired interferonopathies: a reviewОценка роли интерферонов при врожденных и приобретенных интерферонопатияхhttps://orcid.org/0000-0002-1580-60963375-8393OspelnikovaTatiana P.ОспельниковаТатьяна Петровна
Russian Federation

MD, PhD

д.м.н.

ospelnikovat@mail.ruhttps://orcid.org/0000-0003-0787-62519116-7697ShitovaAnna D.ШитоваАнна Денисовна
Russian Federation

Resident

ординатор

countess.iris@yandex.ruhttps://orcid.org/0000-0002-4846-55319252-3080EgorovaOlga N.ЕгороваОльга Николаевна
Russian Federation

MD, PhD

д.м.н.

onegorova@yandex.ruhttps://orcid.org/0009-0005-7411-3694DatsinaMaria V.ДацинаМария Валерьевна
Russian Federation

Student

студентка

mdatsina09@mail.ruhttps://orcid.org/0000-0002-7682-66725389-7907MaximovaMarina Y.МаксимоваМарина Юрьевна
Russian Federation

MD, PhD, Professor

д.м.н., профессор

ncnmaximova@mail.ruI. Mechnikov Research Institute of Vaccines and SeraНаучно-исследовательский институт вакцин и сывороток им. И.И. МечниковаRussian Center for Neurology and NeuroscienceНаучный центр неврологииV.A. Nasonova Research Institute of RheumatologyНаучно-исследовательский институт ревматологии им. В.А. НасоновойI.M. Sechenov First Moscow State Medical University (Sechenov University)Первый Московский государственный медицинский университет имени И.М. Сеченова (Сеченовский Университет)220920268131891980104202611072026Copyright ©; 2026, "Paediatrician" Publishers LLCCopyright ©; 2026, Издательство "Педиатръ"2026"Paediatrician" Publishers LLCИздательство "Педиатръ"https://creativecommons.org/licenses/by-nc-nd/4.0/https://vestnikramn.spr-journal.ru/jour/article/view/18194

Impaired interferon (IFN) production plays a key role in the pathogenesis of a wide range of autoimmune diseases (AIDs), such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), dermatomyositis, and others. This review examines both the physiological functions of IFNs under normal conditions (antiviral defense, regulation of apoptosis and necroptosis, antitumor immunity) and pathological changes in the IFN system associated with AIDs. Particular attention is paid to the concept of type I interferonopathies. Monogenic forms caused by mutations in genes controlling nucleic acid metabolism and IFN signaling pathways, leading to their hyperproduction, are analyzed. Using SLE and dermatomyositis as examples, the key role of excessive IFN signaling in the development of organ damage is demonstrated. Paradoxically, IFN-β drugs are used in MS therapy due to their immunomodulatory effect. A significant portion of this review is devoted to acquired disorders caused by viral infections. Viruses (herpes, hepatitis, SARS-CoV-2) can induce an autoimmune response through molecular mimicry and interfere with the IFN system at various levels: from blocking recognition receptors to epigenetic silencing of interferon-stimulated genes (ISGs). This creates a vicious cycle in which chronic infection and IFN dysregulation exacerbate the autoimmune process. The conclusion emphasizes the dual nature of IFNs: their deficiency increases susceptibility to infections, while excess or dysfunction provokes autoimmunity. A promising direction is the study of IFN biological activity, the search for markers of treatment efficacy, and the development of methods for correcting IFN status (using exogenous IFNs or their inducers) in the complex treatment of AIDs.

Нарушение продукции интерферонов (IFN) играет ключевую роль в патогенезе широкого спектра аутоиммунных заболеваний (АИЗ), таких как системная красная волчанка (СКВ), рассеянный склероз, дерматомиозит и др. В представленном обзоре рассматриваются как физиологические функции IFN в норме (противовирусная защита, регуляция апоптоза и некроптоза, противоопухолевый иммунитет), так и патологические изменения в системе IFN, ассоциированные с АИЗ. Особое внимание уделено концепции интерферонопатий I типа. Анализируются моногенные формы, обусловленные мутациями в генах, контролирующих метаболизм нуклеиновых кислот и сигнальные пути IFN, что ведет к их гиперпродукции. На примере СКВ и дерматомиозита показана ключевая роль избыточной IFN-сигнализации в развитии органных поражений. Парадоксально, но при рассеянном склерозе препараты IFN-β используются в терапии благодаря их иммуномодулирующему действию. Значительная часть обзора посвящена приобретенным нарушениям, вызванным вирусными инфекциями. Вирусы (герпеса, гепатита, SARS-CoV-2) способны индуцировать аутоиммунный ответ через молекулярную мимикрию и вмешиваться в работу системы IFN на различных уровнях — от блокировки рецепторов распознавания до эпигенетического подавления интерферон-стимулируемых генов (ISG). Это создает порочный круг, где хроническая инфекция и дисрегуляция IFN усугубляют аутоиммунный процесс. В заключении подчеркивается двойственная природа IFN: их недостаточность повышает восприимчивость к инфекциям, а избыток или дисфункция провоцируют аутоиммунитет. Перспективными направлениями являются изучение биологической активности IFN, поиск маркеров эффективности терапии и разработка методов коррекции IFN-статуса (применение экзогенных IFN или их индукторов) в комплексном лечении АИЗ.

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