rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.47360/1995-4484-2026-271-278rsp-3946Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL RESEARCHОсобенности цитокинового профиля пациентов с системной красной волчанкой: связь с интерфероновым «автографом»Features of the cytokine profile of patients with systemic lupus erythematosus depending on the presence of an interferon signaturehttps://orcid.org/0000-0003-3057-9175АвдееваА. С.AvdeevaA. S.

Авдеева Анастасия Сергеевна

115522, Москва, Каширское шоссе, 34а

Anastasia Avdeeva

115522, Moscow, Kashirskoye Highway, 34A

9056249400@mail.ruhttps://orcid.org/0000-0001-6404-0042ДиатроптовМ. Е.DiatroptovM. E.

115522, Москва, Каширское шоссе, 34а

115522, Moscow, Kashirskoye Highway, 34A

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

115522, Москва, Каширское шоссе, 34а

115522, Moscow, Kashirskoye Highway, 34A

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

115522, Москва, Каширское шоссе, 34а

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0001-5793-4689ПопковаТ. В.PopkovaT. V.

115522, Москва, Каширское шоссе, 34а

115522, Moscow, Kashirskoye Highway, 34A

https://orcid.org/0000-0003-1053-6952ПанафидинаТ. А.PanafidinaT. A.

115522, Москва, Каширское шоссе, 34а

115522, Moscow, Kashirskoye Highway, 34A

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

115522, Москва, Каширское шоссе, 34а; Минздрава России117997, Москва, ул. Островитянова, 1

115522, Moscow, Kashirskoye Highway, 34A; 117997, Moscow, Ostrovitianova str., 1

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»; ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова»РоссияV.A. Nasonova Research Institute of Rheumatology; N.I. Pirogov Russian National Research Medical UniversityRussian Federation202630062026643271278Copyright © Авдеева А.С., Диатроптов М.Е., Четина Е.В., Горбунова Ю.Н., Попкова Т.В., Панафидина Т.А., Насонов Е.Л., 20262026Авдеева А.С., Диатроптов М.Е., Четина Е.В., Горбунова Ю.Н., Попкова Т.В., Панафидина Т.А., Насонов Е.Л.Avdeeva A.S., Diatroptov M.E., Tchetina E.V., Gorbunova Y.N., Popkova T.V., Panafidina T.A., 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/3946

Цель исследования – оценить цитокиновый профиль пациентов с системной красной волчанкой (СКВ) в зависимости от наличия повышенной экспрессии интерферон (ИФН) стимулированных генов (ИСГ).

Материал и методы

Материал и методы. В анализ было включено 140 пациентов (123 (88%) женщины и 17 (12%) мужчин) с достоверным диагнозом СКВ. Медиана длительности заболевания составила 3,0 [0,3; 12,0] года; SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) – 6,5 [4,0; 10,5], SDI (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) – 0 [0; 2]. ИФН-статус (ИФН-счет) оценивали по экспрессии ИСГ (MX1, RSAD2, EPSTI1) методом полимеразной цепной реакции в режиме реального времени. Исследование 48 цитокинов в сыворотке крови осуществляли методом мультиплексного иммунного анализа на основе суспензионной микрочиповой технологии хМАР (Bio-Plex® 200 Pro Human Cytokine Screening Panel, 48-Plex, Bio-Rad Laboratories, США) согласно инструкциям фирмы-производителя. Контрольную группу составили 13 здоровых доноров, сопоставимых по полу и возрасту с обследованными больными.

Результаты

Результаты. Экспрессия ИСГ и ИФН-счет у пациентов с СКВ были статистически значимо выше по сравнению со здоровыми донорами (p < 0,05). ИФН-«автограф» присутствовал у 103 (81,7%) и отсутствовал у 23 (18,3%) пациентов. При наличии ИФН-«автографа» отмечались более высокий уровень провоспалительных цитокинов (фактор некроза опухоли α (ФНО-α), интерлейкин (ИЛ) 18 и лиганд семейства ФНО, вызывающий апоптоз (TRAIL, TNF-related apoptosis-inducing ligand), хемокинов (ИФНγ-индуцируемый протеин 10 (IP-10, interferon gamma-induced protein 10)), факторов роста (макрофагальный колониестимулирующий фактор (М-КСФ)), антивоспалительных цитокинов (антагонист рецепторов ИЛ-1 (ИЛ-1Ра)) и более низкий уровень фактора роста гепатоцитов.

Заключение

Заключение. Иммунологический фенотип с наличием ИФН-«автографа» характеризуется более высоким уровнем провоспалительных цитокинов (ФНО-α, ИЛ-18, TRAIL), хемокинов (IP-10), факторов роста (М-КСФ), антивоспалительных цитокинов (ИЛ-1Ра), что позволяет говорить о более высокой воспалительной активности у данной группы пациентов.

The aim – to evaluate the cytokine profile of patients with systemic lupus erythematosus (SLE) depending on the presence of increased expression of interferon (IFN) stimulated genes.

Materials and methods

Materials and methods. The analysis included 140 patients (123 (88%) women and 17 (12%) men) with a confirmed diagnosis of SLE. Disease duration was 3.0 [0.3; 12.0] years, SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) score was 6.5 [4.0; 10.5] points, SDI (Systemic Lupus International Collaborating Clinics/ American College of Rheumatology Damage Index) – 0 [0; 2] points. IFN status was assessed by the expression of IFN-stimulated genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction. A study of 48 serum cytokines was performed using a multiplex immunoassay based on xMAP suspension microarray technology (BioPlex® 200 Pro Human Cytokine Screening Panel, 48-Plex, Bio-Rad Laboratories, USA) according to the manufacturer’s instructions. The control group consisted of 13 healthy donors matched for gender and age.

Results

Results. Expression of IFN-stimulated genes and the IFN score were significantly higher in patients with SLE compared to healthy donors (p < 0.05). The IFN signature was present in 103 (81.7%) patients and absent in 23 (18.3%) patients. Patients with the IFN signature had higher levels of proinflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin (IL) 18, TRAIL (TNF-related apoptosis-inducing ligand)), chemokines (IP-10 (interferon gamma-induced protein 10)), growth factors (macrophage colony-stimulating factor (M-CSF), anti-inflammatory cytokines (IL-1 receptor antagonist (IL-1Ra)), and lower levels of hepatocyte growth factor.

Conclusion

Conclusion. The immunological phenotype with the IFN signature is characterized by higher levels of proinflammatory cytokines (TNF-α, IL-18, TRAIL), chemokines (IP-10), growth factors (M-CSF), and anti-inflammatory cytokines (IL-1Ra), which suggests higher inflammatory activity in this group of patients.

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