ArticleImmunology2004
Activation of Epstein-Barr virus by saliva from Sjogren's syndrome patients.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 44 citations in OpenAlex.
- Microbiome immune crosstalk in Sjögren's syndrome: mechanistic insights and translational perspectives.Immunologic research · 2026Review
- The interaction between Epstein-Barr virus and multiple sclerosis genetic risk loci: insights into disease pathogenesis and therapeutic opportunities.Clinical & translational immunology · 2023Review
- Viral infection in thymoma and thymic tumors with autoimmune diseases.Thoracic cancer · 2021Review
- Impact of comorbid Sjögren syndrome in anti-aquaporin-4 antibody-positive neuromyelitis optica spectrum disorders.Journal of neurology · 2021Article
- Innate Immune Modulation Induced by EBV Lytic Infection Promotes Endothelial Cell Inflammation and Vascular Injury in Scleroderma.Frontiers in immunology · 2021Observational
- Role of Viral Infections in the Pathogenesis of Sjögren's Syndrome: Different Characteristics of Epstein-Barr Virus and HTLV-1.Journal of clinical medicine · 2020Review
- Infections as Risk Factor of Sjögren's Syndrome.Open access rheumatology : research and reviews · 2020Review
- Update on Pathogenesis of Sjogren's Syndrome.Current rheumatology reviews · 2017Review
- Presence of Epstein-Barr virus-infected B lymphocytes with thyrotropin receptor antibodies on their surface in Graves' disease patients and in healthy individuals.Autoimmunity · 2014Article
- Epstein-Barr virus in systemic autoimmune diseases.Clinical & developmental immunology · 2013Review
- NF-kappaB-mediated modulation of inducible nitric oxide synthase activity controls induction of the Epstein-Barr virus productive cycle by transforming growth factor beta 1.Journal of virology · 2011Article
- Pathogenetic mechanisms in the initiation and perpetuation of Sjögren's syndrome.Nature reviews. Rheumatology · 2010Review
- B cells in Sjögren's syndrome: indications for disturbed selection and differentiation in ectopic lymphoid tissue.Arthritis research & therapy · 2007Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to examine the mechanism of Epstein-Barr virus (EBV) activation by soluble factors from the inflamed salivary glands of patients with Sjogren's syndrome (SS). Saliva from SS patients was used to examine the regulation of EBV activation by an inflammatory salivary microenvironment. Transient transfection of the EBV-negative salivary gland cell line (HSY) with BZLF1, a trans-activating EBV gene promoter-fusion construct (Zp-luc), was used in this study. The results showed that under conditions where the BZLF1 promoter is activated by potent stimuli, SS saliva (from eight of 12 patients) exerts a significant effect on expression of the luciferase gene. A specific inhibitor of protein kinase C did not affect the SS saliva-induced Zp-luc activity, whereas treatment with inhibitors of calmodulin, calcineurin and IP3, dose-dependently decreased this induction. Transforming growth factor beta1 (TGF-beta1), which is known to be expressed in SS salivary glands, dose-dependently induced Zp-luc activity. Hence, these results demonstrate the activation of EBV by SS saliva and suggest that EBV activation at the inflammatory site may occur in the presence of TGF-beta1 via triggering of the mitogen-activated protein kinase (MAPK) kinase signalling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.