2024 / 03

DOI: 10.24075/brsmu.2024.027

OPINION

Interferon signature in the development of SLE: molecular mechanisms, approaches to diagnosis and treatment

Nakonechnaya TO1, Shagina IA2,3, Myshkin MYu2,3, Mutovina ZYu4, Ryazantseva EV4, Chudakov DM1,2, Turchaninova MA2,3, Britanova OV2,3
About authors

1 Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry Russian Academy of Sciences, Moscow, Russia

2 Pirogov Russian National Research Medical University, Moscow, Russia

3 LLC MiLaboratory, Moscow, Russia

4 Department of Rheumatology, City Clinical Hospital No. 52 of the Department of Health, Moscow, Russia

Correspondence should be addressed: Olga V. Britanova
Miklouho-Maklaya, s. 16/10, 117997, Moscow, Russia; moc.liamg@natirblo

About paper

Financing: the study was supported by a grant from the Moscow Government (NIP No. 2412-63/22-1 dated May 13, 2022), sponsored by the Moscow Center for Innovative Technologies in Healthcare.

Author contribution: Myshkin MYu — literature analysis; Mutovina ZYu, Shagina IA — data collection in the field of rheumatology and medicine; Chudakov DM — concept, Turchaninova MA — analysis and interpretation of scientific data; Ryazantseva EV, Kazhdan MA — manuscript proofreading, Britanova OV, Nakonechnaya TO — literature analysis and manuscript preparation.

Received: 2024-06-24 Accepted: 2024-06-28 Published online: 2024-06-30
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Fig. 1. Development of systemic lupus erythematosus
Fig. 2. Pattern of type I interferon production
Fig. 3. Type I IFN signaling pathway: IFGF3 — IFN-stimulated factor 3, ISRE — IFN-stimulated response, IFR9 — IFN regulatory factor 9, GAS — gamma-activated sequence, SIN3A-SIN3 — transcription regulator homolog, CXCL9 — ligand 9 CXC chemokines, JAD — 25-oligoadenylate synthesis, MX1 — IFN-induced GTP-binding protein 1, P — phosphate [66]