Interleukin-17 as a predictor of subclinical synovitis in the remission state of rheumatoid arthritis

Misra, Satya Ranjan; Mondal, Sumantro; Chatterjee, Sulagna; Dutta, Satarupa; Sinha, Debanjali; Bhattacharjee, Dipanjan; Lahiri, Debasish; Ghosh, Alakendu

doi:10.1016/j.cyto.2022.155837

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…С другой стороны, ИЛ-17A может запускать ВСП через систему JAK-STAT. Передача сигнала ИЛ-17A через JAK2/STAT1 и STAT3 имеет большое значение в активации астроцитов в процессе асептического нейронального воспаления [68,69]. Активация этого пути увеличивает экспрессию сосудистого эндотелиального фактора роста, ответственного за неоангигенез и проницаемость ГЭБ [70,71].…”

Section: рис 2 молекулярные аспекты развития гипералгезии: фно-α -фак...unclassified

Molecular mechanisms of the development of the phenomena of peripheral and central sensitization in rheumatoid arthritis

Potapova¹

2023

Naučno-praktičeskaâ revmatologiâ

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Modern tactics for the treatment of rheumatoid arthritis is aimed at achieving remission or low activity of the disease, the maximum elimination of the manifestations of the disease and the restoration of physical and social activity of patients. At the same time, despite the wide range of the most modern pathogenetic agents, a good therapeutic response can’t be obtained in all cases. A difficult problem is the so-called rheumatoid arthritis RA (difficult to treat), in which two or more sequentially prescribed genetically engineered biological drugs or JAK inhibitors are ineffective. One of the important factors negatively affecting the outcome of RA treatment are functional disorders of the nociceptive system, such as peripheral and central sensitization. These phenomena, associated with persistent activation of nociceptive neurons and the development of nociplastic changes, are caused by systemic autoimmune inflammation and the influence of various cytokines and chemokines on the neuronal membrane. This review considers the molecular biological aspects of the formation of peripheral and central sensitization in RA, with a separate analysis of the pathogenetic role of individual interleukins.

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Section: рис 2 молекулярные аспекты развития гипералгезии: фно-α -фак...unclassified

Molecular mechanisms of the development of the phenomena of peripheral and central sensitization in rheumatoid arthritis

Potapova¹

2023

Naučno-praktičeskaâ revmatologiâ

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“…По данным клинических исследований, в сыворотке и синовиальной жидкости концентрация ИЛ-17А существенно выше, чем у пациентов с остеоартритом (а также с подагрой и травматическим артритом) и в контроле [83][84][85][86][87][88][89][90][91][92], коррелирует с активностью (DAS28-CРБ (Disease Activity Score 28 с определением уровня С-реактивного белка)), длительностью [83] и тяжестью РА [89][90][91][92], гиперпродукцией антител к циклическим цитруллинированным белкам (АЦБ) [84], развитием субклинического синовита [86] и деструкцией суставов [87]. Отмечено увеличение спонтанной секреции ИЛ-17 в синовиальной ткани при РА по сравнению с пациентами с остеоартритом и контролем [57,93].…”

Section: роль интерлейкина 17 в патогенезе раunclassified

The role of interleukin 17 in the pathogenesis of rheumatoid arthritis. Are there any prospects for the use of IL-17 inhibitors?

Насонов

Авдеева²,

Коротаева³

et al. 2023

Naučno-praktičeskaâ revmatologiâ

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Rheumatoid arthritis (RA) is an immunoinflammatory rheumatic disease (IMRI) characterized by chronic erosive arthritis and systemic damage to internal organs, leading to early disability and reduced life expectancy in patients. Thanks to the progress in the study of the mechanisms of the development of the IVRI and industrial biotechnology, new anti-inflammatory drugs have been created, the use of which has significantly increased the effectiveness of the pharmacotherapy of RA. However, the possibilities of pharmacotherapy for RA are limited, since all genetically engineered biological drugs (GEBDs), regardless of the mechanism of action, have approximately the same effectiveness in achieving remission. It is believed that the relatively unsatisfactory results of RA therapy are due to the heterogeneity of the mechanisms of inflammation. and pain. The significance of the Th17 type of immune response in the pathogenesis of RA, the results of controlled studies of IL-17 inhibitors, and the advisability of further studying the effectiveness of these drugs in patients with certain RA phenotypes are discussed.

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“…The Janus-activated kinase Signal transducers and activators of transcription (JAK-STAT), TLR, Ras, and other signaling pathways are located upstream of a variety of inflammatory factors. These pathways play the dual role of cytokine signaling and transcriptional activation of target genes and participate in several processes such as the regulation of the autoimmune inflammatory responses in the body [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Exploration of the molecular mechanism guiding Xinfeng capsule regulatory mechanism for rheumatoid arthritis inflammation

Zhu

2024

Am J Transl Res

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Objectives: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the joint synovium. The traditional Chinese medicine Xinfeng capsule (XFC) has a remarkable alleviating effect on inflammatory symptoms, such as joint pain and swelling, in patients with RA. However, the underlying mechanism of action remains to be elucidated. This study intended to conduct network pharmacology, animal experiments, data mining, and molecular docking to explore the molecular mechanism through which XFC can improve the inflammatory symptoms of RA. Methods: The Apriori association rules and a random walk model were employed to evaluate the effect of XFC on the clinical inflammatory indexes of RA. The active ingredients and the potential target genes of XFC were obtained from public databases. Based on the search tool for recurring instances of neighboring genes (STRING) database, the Database for Annotation, Visualization and Integrated Discovery (DAVID) database, Cytoscape software, and molecular docking method, the molecular mechanism by which XFC acts on RA was also analyzed. Finally, an adjuvant arthritis rat model was established to verify the effects of XFC on inflammationrelated signaling pathways and inflammatory factors. Results: XFC significantly reduced the level of C-reactive protein (CRP), vascular endothelial growth factor (VEGF), and the erythrocyte sedimentation rate (ESR). The docking space structures of the active ingredients in XFC, namely triptolide and quercetin, and the key targets were stable. Inflammation-related biological processes were identified as the key factors involved in the development of RA, and the regulation of the toll-like receptor (TLR) signaling pathway may be the key link for XFC toward improving the inflammatory state of RA. The expression levels of toll-like receptor 4 (TLR4), myeloid differentiation primary response protein MyD88 (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK1), TNF receptor-associated factor 6 (TRAF6), TGF-beta-activated kinase 1 (TAK1), phospho-Inhibitor of NF-κB kinaseβ (p-IKKβ), phospho-Nuclear factor-k-gene binding (p-NF-κB), and interleukin-1β (IL-1β) can all be decreased by XFC. XFC improves joint inflammation symptoms by lowering pro-inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (INF-γ) levels. Conclusions: XFC could effectively improve the clinical inflammatory indexes of RA. The active ingredients of XFC improved the inflammatory state of RA by regulating the TLR-signaling pathway.

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Interleukin-17 as a predictor of subclinical synovitis in the remission state of rheumatoid arthritis

Cited by 6 publications

References 32 publications

Molecular mechanisms of the development of the phenomena of peripheral and central sensitization in rheumatoid arthritis

Molecular mechanisms of the development of the phenomena of peripheral and central sensitization in rheumatoid arthritis

The role of interleukin 17 in the pathogenesis of rheumatoid arthritis. Are there any prospects for the use of IL-17 inhibitors?

Exploration of the molecular mechanism guiding Xinfeng capsule regulatory mechanism for rheumatoid arthritis inflammation

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