ArticleJournal of autoimmunity2013
A link between interferon and augmented plasmin generation in exocrine gland damage in Sjögren's syndrome.
Article in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Exosomes in corneal diseases: advances in diagnosis and therapy.Frontiers in cell and developmental biology · 2026Review
- Macrophage polarization in Sjögren's syndrome: from mechanisms to therapeutic translation.Frontiers in immunology · 2026Review
- Review
- Fecal metabolomic analysis of the role of gut microbiota and short-chain fatty acids in the therapeutic mechanism of Timosaponin AIII in Sjögren's syndrome.Clinical rheumatology · 2025Article
- Pharmacological Mechanisms of CheReCunJin Formula in Ameliorating Sjögren's Syndrome: Suppression of IL-17 Signal-Mediated Inflammatory Cascade.Journal of inflammation research · 2025Article
- Multi-Omics Mendelian Randomization Identifies Therapeutic Targets for Sjögren's Disease with Clinical and Bayesian Validation.Journal of inflammation research · 2025Article
- Article
- Ocular microvascular alteration in Sjögren's syndrome treated with hydroxychloroquine: an OCTA clinical study.Therapeutic advances in chronic disease · 2023Article
- Defining the Role of Monocytes in Sjögren's Syndrome.International journal of molecular sciences · 2022Review
- MSC-Derived Small Extracellular Vesicles Attenuate Autoimmune Dacryoadenitis by Promoting M2 Macrophage Polarization and Inducing TregsFrontiers in immunology · 2022Article
- Optical Coherence Tomography Angiography Biomarkers of Retinal Thickness and Microvascular Alterations in Sjogren's Syndrome.Frontiers in neurology · 2022Article
- Triptolide reduces salivary gland damage in a non-obese diabetic mice model of Sjögren's syndrome via JAK/STAT and NF-κB signaling pathways.Journal of clinical biochemistry and nutrition · 2021Article
- The Involvement of Innate and Adaptive Immunity in the Initiation and Perpetuation of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- HMSC-Derived Exosome Inhibited Th2 Cell Differentiation via Regulating miR-146a-5p/SERPINB2 Pathway.Journal of immunology research · 2021Observational
- Building a Functional Salivary Gland for Cell-Based Therapy: More than Secretory Epithelial Acini.Tissue engineering. Part A · 2020Review
- Contributions of Major Cell Populations to Sjögren's Syndrome.Journal of clinical medicine · 2020Review
- Long non‑coding RNAs are novel players in oral inflammatory disorders, potentially premalignant oral epithelial lesions and oral squamous cell carcinoma (Review).International journal of molecular medicine · 2020Review
- Associations of Anti-Aquaporin 5 Autoantibodies with Serologic and Histopathological Features of Sjögren's Syndrome.Journal of clinical medicine · 2019Article
- The Clinical Relevance of IL-17-Producing CD4+CD161+ Cell and Its Subpopulations in Primary Sjögren's Syndrome.Journal of immunology research · 2015Article
- The challenge of treating orphan disease.Clinical reviews in allergy & immunology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Sjögren's syndrome is an autoimmune disease that targets exocrine glands, but often exhibits systemic manifestations. Infiltration of the salivary and lacrimal glands by lymphoid and myeloid cells orchestrates a perpetuating immune response leading to exocrine gland damage and dysfunction. Th1 and Th17 lymphocyte populations and their products recruit additional lymphocytes, including B cells, but also large numbers of macrophages, which accumulate with disease progression. In addition to cytokines, chemokines, chitinases, and lipid mediators, macrophages contribute to a proteolytic milieu, underlying tissue destruction, inappropriate repair, and compromised glandular functions. Among the proteases enhanced in this local environment are matrix metalloproteases (MMP) and plasmin, generated by plasminogen activation, dependent upon plasminogen activators, such as tissue plasminogen activator (tPA). Not previously associated with salivary gland pathology, our evidence implicates enhanced tPA in the context of inflamed salivary glands revolving around lymphocyte-mediated activation of macrophages. Tracking down the mechanism of macrophage plasmin activation, the cytokines IFNγ and to a lesser extent, IFNα, via Janus kinase (JAK) and signal transducer and activator of transcription (STAT) activation, were found to be pivotal for driving the plasmin cascade of proteolytic events culminating in perpetuation of the inflammation and tissue damage, and suggesting intervention strategies to blunt irreversible tissue destruction.
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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.