A comprehensive review of Sjögren's syndrome: classification criteria, risk factors, and signaling pathways DOI Creative Commons

Ting Zhao,

Runrun Zhang, Zhaofu Li

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(17), P. e36220 - e36220

Published: Aug. 15, 2024

Sjögren's syndrome (SS) is a chronic autoimmune disease that affects the exocrine glands and may lead to range of systemic symptoms impact various organs. Both innate adaptive immune pathways might trigger disease. Studying signaling underlying SS crucial for enhancing diagnostic therapeutic effectiveness. poses an ongoing challenge medical professionals owing limited options available. This review offers comprehensive understanding intricate nature SS, encompassing classification criteria, risk factors, in immunity inflammation. The advancements summarized herein have potential spark new avenues research into SS.

Language: Английский

The crucial regulatory role of type I interferon in inflammatory diseases DOI Creative Commons
Ling Ji, Tianle Li,

Huimin Chen

et al.

Cell & Bioscience, Journal Year: 2023, Volume and Issue: 13(1)

Published: Dec. 20, 2023

Type I interferon (IFN-I) plays crucial roles in the regulation of inflammation and it is associated with various inflammatory diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), periodontitis, impacting people's health quality life. It well-established that IFN-Is affect immune responses factors by regulating some signaling. However, currently, there no comprehensive overview regulatory role IFN-I distinctive pathways as well diseases. This review aims to provide a narrative involvement different signaling pathways, mainly mediating related key specific targets cascades influence progression As such, we suggested induce through stimulation certain which displays possible efficient treatment methods provides reference for precise control

Language: Английский

Citations

31
The pseudorabies virus UL13 protein kinase triggers phosphorylation of the RNA demethylase FTO, which is associated with FTO-dependent suppression of interferon-stimulated gene expression DOI Creative Commons
Ruth Verhamme, Robert J. J. Jansens, Jianheng Liu

et al.

Journal of Virology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

ABSTRACT Alpha-ketoglutarate-dependent dioxygenase, also known as fat mass and obesity-associated protein (FTO), is an RNA demethylase that mediates the demethylation of N 6 ,2-O-dimethyladenosine (m6Am) -methyladenosine (m6A). Both m6Am m6A are prevalent modifications in mRNA affect different aspects transcript biology, including splicing, nuclear export, translation efficiency, degradation. The role FTO during (herpes) virus infection remains largely unexplored. In this study, we show UL13 kinase alphaherpesvirus pseudorabies (PRV) triggers phosphorylation FTO. primary epithelial cells, depletion leads to increased expression antiviral interferon-stimulated genes (ISGs) FTO-dependent suppression ISG expression. Although PRV suppresses levels host small RNA, independent UL13. current data highlight important regulator suggest UL13-mediated may serve a previously unrecognized viral strategy suppress interferon response. IMPORTANCE modification pathways play roles diverse cellular processes life cycles. previous studies have demonstrated alphaherpesviruses can substantially influence modifications, such m6A, impact on epitranscriptome machinery present work reports (PRV), alphaherpesvirus, m6Am/m6A eraser correlates with UL13- gene (ISG) Furthermore, pronounced reduction snRNA induces writer PCIF1. These reveal manipulation FTO, UL13-induced evasion strategy.

Language: Английский

Citations

1
Type I Interferons in Autoimmunity: Implications in Clinical Phenotypes and Treatment Response DOI Open Access

Ana Carolina Londe,

Ruth Fernandez‐Ruiz, Paulo Rogério Júlio

et al.

The Journal of Rheumatology, Journal Year: 2023, Volume and Issue: 50(9), P. 1103 - 1113

Published: July 1, 2023

Type I interferon (IFN-I) is thought to play a role in many systemic autoimmune diseases. IFN-I pathway activation associated with pathogenic features, including the presence of autoantibodies and clinical phenotypes such as more severe disease increased activity damage. We will review potential drivers dysregulation 5 prototypic diseases: lupus erythematosus, dermatomyositis, rheumatoid arthritis, primary Sjögren syndrome, sclerosis. also discuss current therapeutic strategies that directly or indirectly target system.

Language: Английский

Citations

22
Inflammatory cytokines and their potential role in Sjogren’s syndrome risk: insights from a mendelian randomization study DOI Creative Commons
Wenbin Shi,

Yuli Xu,

Anan Zhang

et al.

Advances in Rheumatology, Journal Year: 2024, Volume and Issue: 64(1)

Published: Feb. 16, 2024

Abstract Aim This study aimed to investigate the causal impact of inflammatory cytokines on Sjogren’s Syndrome (SS) and identify potential biomarkers for SS clinical management using Mendelian Randomization (MR). Materials methods Leveraging GWAS summary data SS, we executed first two-sample MR analysis. Genetic variants from prior GWASs associated with circulating served as instrumental variables (IVs). Data regarding were analyzed Olink Target-96 Inflammation panel, synthesizing 14,824 participants. statistics procured UK Biobank, focusing samples European ancestry. To discern relationship between several methodologies, including inverse variance weighted (IVW) MR-Egger regression, applied. Results After rigorous IV quality control, 91 incorporated into The IVW analysis identified 8 a positive association SS: Axin-1 (OR 2.56, 95% CI 1.07–6.10), T-cell surface glycoprotein CD5 1.81, 1.08–3.02), CUDP1 1.61, 1.00-2.58), CXCL10 1.92, 1.25–2.95), IL-4 2.18, 1.22–3.91), IL-7 2.35, 1.27–4.33), MCP-2 1.27, 1.05–1.54), TNFRSF9 1.83, 1.03–3.24), suggesting their in increasing risk. Conclusion Our conducted through MR, various risk, validating some previous research results offering new SS. However, these findings necessitate further validation exploration precise role onset progression

Language: Английский

Citations

7
PANoptosis Features, a Humanized NSG Murine Model of Sjogren's Syndrome DOI
Yiying Yang, Huali Zhang, Xiaoyu Xiao

et al.

DNA and Cell Biology, Journal Year: 2024, Volume and Issue: 43(5), P. 207 - 218

Published: April 18, 2024

Sjogren's syndrome (SS) is a complex systemic autoimmune disease. This study aims to elucidate humanized NOD-Prkdc

Language: Английский

Citations

6
Intermittent hypoxia exacerbates anxiety in high-fat diet-induced diabetic mice by inhibiting TREM2-regulated IFNAR1 signaling DOI Creative Commons

Wenyu Ni,

Yun Niu,

Sitong Cao

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: July 2, 2024

Abstract Background Type 2 diabetes mellitus (T2DM) and obstructive sleep apnea (OSA) are mutual risk factors, with both conditions inducing cognitive impairment anxiety. However, whether OSA exacerbates anxiety in patients T2DM remains unclear. Moreover, TREM2 upregulation has been suggested to play a protective role attenuating microglia activation improving synaptic function mice. The aim of this study was explore the regulatory mechanisms anxiety-like behavioral changes mice combined T2DM. Methods A model developed by treating 60% kcal high-fat diet (HFD) intermittent hypoxia (IH). Spatial learning memory capacity were investigated. Neuronal damage brain determined quantity synapses density, number morphology microglia, pro-inflammatory factors. For mechanism exploration, an vitro generated co-treating high glucose (HG) IH. Regulation on IFNAR1-STAT1 pathway RNA sequencing qRT-PCR. Results Our results showed that HFD exhibited significant dysfunction behavior, accompanied loss. Furthermore, enhanced microglial phagocytosis observed. IH found significantly aggravate HG treatment may potentially involve promotion upregulation, which turn attenuates proinflammatory inhibiting pathway. Conversely, reduction IH-co-treated HG-treated resulted further consequently increased activation. Conclusions upregulated induced leading causing deficits. inT2DM exerted negative regulation Mice exacerbated via downregulation TREM2, heightened increasing microglia. Graphical

Language: Английский

Citations

5
Profiling Type I and II Interferon Responses Reveals Distinct Subgroups of Pediatric Patients with Autoinflammatory Disorders DOI Creative Commons

Anaïs Nombel,

Magali Perret, Sophie Trouillet‐Assant

et al.

Journal of Allergy and Clinical Immunology Global, Journal Year: 2025, Volume and Issue: 4(2), P. 100450 - 100450

Published: March 8, 2025

Elevation of type I interferon (IFN-I) is characteristic a group diseases known as interferonopathies. Several technologies are available to monitor IFN-I, but there no consensus on their routine use in medical laboratories. We aimed compare the performance two for this purpose: NanoString, which monitors messenger RNA expression interferon-stimulated genes (ISGs), and Simoa, quantifies IFN-α2 protein an ultrasensitive way. also designed NanoString assay II ISGs tested its value discriminate clinical conditions. A total 196 samples from patients with associated or not IFN-I pathway activation were analyzed by Simoa. The comparison between score Simoa revealed r 2 coefficient 0.55. identified IFI27, IFI44L, SIGLEC1 most closely related concentration. Nineteen had positive undetectable IFN-α2. These according IFN-II score, pointing primary ISG inducer corresponding patients. By measuring scores subset systemic lupus erythematosus juvenile idiopathic arthritis, we subgroups whom dominant. Both quantification reliably distinguish interferonopathies other diseases. Type interferons induce different transcriptomic signatures vitro vivo, our results highlight monitoring both interferon-related

Language: Английский

Citations

0
Type I Interferons and Systemic Lupus Erythematosus DOI

向阳 张

Medical Diagnosis, Journal Year: 2025, Volume and Issue: 15(02), P. 140 - 147

Published: Jan. 1, 2025

Language: Английский

Citations

0
Immunohistochemical analysis reveals higher Myxovirus resistance protein 1 expression and increased macrophage count in placentas from patients with systemic rheumatic diseases DOI Creative Commons
Juan J. Fierro, Mirthe H. Schoots, S.C. Liefers

et al.

Rheumatology International, Journal Year: 2025, Volume and Issue: 45(4)

Published: April 4, 2025

Language: Английский

Citations

0
Rapid Detection of Anti‐IFN‐α2 Autoantibodies Using a New Automated VIDAS Assay Prototype DOI Creative Commons
Sylvie Pons,

Laurence Generenaz,

Adrian Gervais

et al.

European Journal of Immunology, Journal Year: 2025, Volume and Issue: 55(4)

Published: April 1, 2025

Autoantibodies neutralizing Type I interferons increase the risk of severe viral diseases and are linked to autoimmune conditions. The automated VIDAS assay is suitable for anti-IFN-α2 IgGs quantification, offering a swift, reliable, user-friendly, single test clinical management.

Language: Английский

Citations

0