rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.47360/1995-4484-2025-95-103rsp-3706Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL RESEARCHКлиническое значение интерферонового статуса у пациентов с системной красной волчанкой. Предварительные данныеClinical significance of interferon status in patients with systemic lupus erythematosus. Preliminary datahttps://orcid.org/0000-0003-1053-6952ПанафидинаТ. А.PanafidinaT. A.

Панафидина Татьяна Александровна.

115522, Москва, Каширское шоссе, 34а

Tatiana A. Panafidina.

115522, Moscow, Kashirskoye Highway, 34A

panafidina@inbox.ruhttps://orcid.org/0000-0001-5793-4689ПопковаТ. В.PopkovaT. V.

115522, Москва, Каширское шоссе, 34а

Tatiana V. Popkova.

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0002-2024-6927ГорбуноваЮ. Н.GorbunovaYu. N.

115522, Москва, Каширское шоссе, 34а

Yulia N. Gorbunova.

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0003-1147-5936КондратьеваЛ. В.KondratyevaL. V.

115522, Москва, Каширское шоссе, 34а

Liubov V. Kondratyeva.

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0001-7312-2349ЧетинаЕ. В.TchetinaE. V.

115522, Москва, Каширское шоссе, 34а

Elena V. Tchetina.

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0003-3057-9175АвдееваА. С.AvdeevaA. S.

115522, Москва, Каширское шоссе, 34а

Anastasia S. Avdeeva.

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0002-6068-3080ЛилаА. М.LilaA. M.

115522, Москва, Каширское шоссе, 34а; 125993, Москва, ул. Баррикадная, 2/1, стр. 1

Aleksander M. Lila.

115522, Moscow, Kashirskoye Highway, 34A; 125993, Moscow, Barrikadnaya str., 2/1, building 1

https://orcid.org/0000-0002-1598-8360НасоновЕ. Л.NasonovE. L.

115522, Москва, Каширское шоссе, 34а

Evgeny L. Nasonov.

115522, Moscow, Kashirskoye Highway, 34A

ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»РоссияV.A. Nasonova Research Institute of RheumatologyRussian FederationФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»; ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава РоссииРоссияV.A. Nasonova Research Institute of Rheumatology; Russian Medical Academy of Continuous Professional Education of the Ministry of Healthcare of the Russian FederationRussian Federation20250203202563195103Copyright © Панафидина Т.А., Попкова Т.В., Горбунова Ю.Н., Кондратьева Л.В., Четина Е.В., Авдеева А.С., Лила А.М., Насонов Е.Л., 20252025Панафидина Т.А., Попкова Т.В., Горбунова Ю.Н., Кондратьева Л.В., Четина Е.В., Авдеева А.С., Лила А.М., Насонов Е.Л.Panafidina T.A., Popkova T.V., Gorbunova Y.N., Kondratyeva L.V., Tchetina E.V., Avdeeva A.S., Lila A.M., Nasonov E.L.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://rsp.mediar-press.net/rsp/article/view/3706

Исследования, раскрывающие патогенез системной красной волчанки (СКВ), в качестве основных факторов, способствующих развитию заболевания, определили два важнейших семейства медиаторов – интерферон (ИФН) I типа и аутоантитела, направленные на нуклеиновые кислоты и белки, связанные с ними.

Цель исследования – оценить особенности интерферонового статуса у пациентов с системной красной волчанкой, выявить взаимосвязь с клиническими и иммунологическими проявлениями болезни.

Материал и методы

Материал и методы. В одноцентровое ретроспективно-проспективное наблюдательное исследование было включено 76 пациентов (86% женщин) с достоверным диагнозом СКВ, соответствующим критериям SLICC (Systemic Lupus International Collaborating Clinics) 2012 г. Медиана возраста на момент включения составила 33 [25; 43] года, длительности заболевания – 2,3 [0,2; 11,0] года, SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) – 7 [4; 11] баллов, индекса повреждения SDI (SLICC Damage Index) – 0 [0; 2] баллов. Для оценки ИФН «автографа» были отобраны 3 ИФН-стимулированных гена (ИСГ) – MX1, RSAD2, EPSTI1. ИФН «автограф» рассчитан как среднее значение экспрессии трех выбранных генов. У пациентов ИФН «автограф» считался положительным при среднем значении генной экспрессии, превышающем среднее значение экспрессии генов у доноров. Контрольную группу составили 20 доноров, не имеющих ревматических заболеваний и активной инфекции, сопоставимых по полу и возрасту с обследованными больными.

Результаты

Результаты. ИФН «автограф» присутствовал у 72% пациентов с СКВ, которые были разделены на две подгруппы – с ИФН «автографом» и без него. Пациенты с ИФН «автографом» по сравнению с теми, кто его не имел, были моложе на момент включения в исследование (медиана возраста – 31 [25; 41] и 40 [32; 49] лет соответственно), у них реже определялась ремиссия СКВ (в 2% и 19% случаев соответственно), выявлялись более высокие концентрации антител к двуспиральной ДНК (219,8 [120,3; 729,3] и 131,0 [46,6; 265,9] МЕ/мл соответственно), чаще встречался титр антинуклеарного фактора (АНФ) ≥1/1280 (84% и 52% соответственно), было ниже количество лейкоцитов (4,2 [3,2; 5,6] и 6,6 [4,2; 8,8] тыс. соответственно) и лимфоцитов крови (1,3 [0,8; 1,8] и 2,0 [1,2; 3,2] тыс. соответственно), чаще выявлялись поражение кожи (31% и 19% соответственно), гематологические нарушения (56% и 29% соответственно) и лейкопения (53% и 24% соответственно), реже встречались дислипидемия (13% и 38% соответственно) и артериальная гипертензия (24% и 52% соответственно; p<0,05 во всех случаях). Связи с лекарственной терапией, назначавшейся для лечения СКВ, и экспрессией ИСГ не обнаружено.

Выводы

Выводы. ИФН «автограф» – это маркер определенного варианта СКВ, который встречается у пациентов молодого возраста и характеризуется преобладанием кожных, гематологических и иммунологических нарушений. Связи со стандартной терапией и уровнем экспрессии определённых ИСГ не обнаружено.

Background

Background. Studies of systemic lupus erythematosus (SLE) pathogenesis have identified two major families of mediators: type I interferon (IFN-I) and autoantibodies to nucleic acids and their proteins, as the main factors contributing to the development of the disease. Against a background of genetic predisposition, a trigger stimulus, possibly microbial, induces the production of IFN-I, autoantibodies or, more likely, both, leading to inflammation. The interaction of cells of the innate and adaptive immune system are involved in the autoimmune response with the development of a variety of clinical manifestations of SLE.

The aim of our study was to describe clinical and immunological characteristics of systemic lupus erythematosus depending on interferon gene signature (IFNGS).

Material and methods This observational retrospective-prospective study included 76 patients (86% women, median aged 33 [25; 43] years (median [interquartile range 25%; 75%]), with a definite diagnosis of SLE (SLICC (Systemic Lupus International Collaborating Clinics), 2012) attending a routine visit at our Clinic between February 2021 and June 2024. Baseline demographics, disease characteristic, organ system involvement/damage were analysed descriptively according to SLE Disease Activity Index 2000 (SLEDAI-2K), SLICC Damage Index (SDI) and IFNGS status (high/low). IFN status was assessed by the expression of IFN-inducible genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction. IFNGS was calculated as the average expression value of three selected genes. In patients, IFNGS was considered high when the average value of gene expression exceeded the average value of gene expression in donors. The control group consisted of 20 healthy donors comparable in sex and age with the SLE patients.

Results

Results. The median disease duration was 2.3 [0.2; 11.0] years, SLEDAI-2K – 7 [4; 11], SDI – 0 [0; 2]. IFNGS-high was detected in 72% of SLE patients. IFNGS-high patients were younger at the time of inclusion (31 [25; 41] and 40 [32; 49] years, respectively), had less frequent remission of SLE (SLEDAI-2K=0) (2% and 19%, respectively), and higher concentrations of anti-dsDNA (219.8 [120.3; 729.3] and 131.0 [46.6; 265.9] IU/ml, respectively; normal <100 IU/ml), ANF titer ≥1/1280 (84% and 52%, respectively), lower absolute count of blood leukocytes (4.2 [3.2; 5.6] and 6.6 [4.2; 8.8]×109/L, respectively) and lymphocytes (1.3 [0.8; 1.8] and 2.0 [1.2; 3.2]×109/L, respectively; p<0,05 in all cases). Of the criterion and non-criteria manifestations of SLE the greater proportions of IFNGS-high versus IFNGS-low patients had haematological (56% and 29%, respectively), primarily leukopenia (53% and 24%, respectively) and dermal (31% and 19, respectively %) involvement (p<0,05 in all cases).

Conclusions

Conclusions. Elevated type I IFN signalling is a marker of a certain type of SLE patients – young age with predominant skin, haematological and immunological disorders. No association with standard therapy and the expression level of certain IFNGS was found.

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The authors declare that there are no conflicts of interest present.