ReviewJournal of clinical medicine2020
Role of Viral Infections in the Pathogenesis of Sjögren's Syndrome: Different Characteristics of Epstein-Barr Virus and HTLV-1.
Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Evidence that autoantibody production may be driven by acute Epstein-Barr virus infection in Sjögren's disease.Annals of the rheumatic diseases · 2024Article
- Primary Sjögren's syndrome: new perspectives on salivary gland epithelial cells.European journal of medical research · 2024Review
- Long Non-Coding RNAs in Sjögren's Disease.International journal of molecular sciences · 2024Review
- Current developments and opportunities of pluripotent stem cells-based therapies for salivary gland hypofunction.Frontiers in cell and developmental biology · 2024Review
- Enterovirus A71 infection-induced dry eye-like symptoms by damaging the lacrimal glands.Frontiers in cellular and infection microbiology · 2024Article
- The role of cytokines from salivary gland epithelial cells in the immunopathology of Sjögren's syndrome.Frontiers in immunology · 2024Review
- Non-Coding RNA in Salivary Extracellular Vesicles: A New Frontier in Sjögren's Syndrome Diagnostics?International journal of molecular sciences · 2023Article
- The Spectrum of Extraglandular Manifestations in Primary Sjögren's Syndrome.Journal of personalized medicine · 2023Review
- Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren's Syndrome: Identification of New Targets.International journal of molecular sciences · 2022Review
- Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome?Immune network · 2022Review
- Review
- LAMP3 inhibits autophagy and contributes to cell death by lysosomal membrane permeabilization.Autophagy · 2022Article
- Review
- The role of virus infections in Sjögren's syndrome.Frontiers in immunology · 2022Review
- The Clinical and Immunological Activity Depending on the Presence of Interferon γ in Primary Sjögren's Syndrome-A Pilot Study.Journal of clinical medicine · 2021Article
- The Role of Interferons in the Pathogenesis of Sjögren's Syndrome and Future Therapeutic Perspectives.Biomolecules · 2021Review
- Making Sense of Intracellular Nucleic Acid Sensing in Type I Interferon Activation in Sjögren's Syndrome.Journal of clinical medicine · 2021Review
- Management of Sjögren's Syndrome: Present Issues and Future Perspectives.Frontiers in medicine · 2021Review
- Special Issue-"Diseases of the Salivary Glands".Journal of clinical medicine · 2020Article
- Contributions of Major Cell Populations to Sjögren's Syndrome.Journal of clinical medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Viruses are possible pathogenic agents in several autoimmune diseases. Sjögren's syndrome (SS), which involves exocrine dysfunction and the appearance of autoantibodies, shows salivary gland- and lacrimal gland-oriented clinical features. Epstein-Barr virus (EBV) is the most investigated pathogen as a candidate that directly induces the phenotype found in SS. The reactivation of the virus with various stimuli induced a dysregulated form of EBV that has the potential to infect SS-specific B cells and plasma cells that are closely associated with the function of an ectopic lymphoid structure that contains a germinal center (GC) in the salivary glands of individuals with SS. The involvement of human T-cell leukemia virus type 1 (HTLV-1) in SS has been epidemiologically established, but the disease concept of HTLV-1-associated SS remains unexplained due to limited evidence from basic research. Unlike the cell-to-cell contact between lymphocytes, biofilm-like structures are candidates as the mode of HTLV-1 infection of salivary gland epithelial cells (SGECs). HTLV-1 can infect SGECs with enhanced levels of inflammatory cytokines and chemokines that are secreted from SGECs. Regardless of the different targets that viruses have with respect to affinitive lymphocytes, viruses are involved in the formation of pathological alterations with immunological modifications in SS.
Indexed as
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What OpenQuestion holds
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.