ArticleClinical and experimental immunology2019
Interleukin-17 and -22 synergy linking inflammation and EMT-dependent fibrosis in Sjögren's syndrome.
Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Composition and regulation of the immune microenvironment of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2022Pooled it
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
- JAK inhibitor tofacitinib alleviates secretory dysfunction and Th17/Treg imbalance in a Sjögren's disease murine model.Annals of medicine · 2026Article
- p16-mediated G0/G1 cell cycle arrest leads to SASP and fibrosis in Fuchs endothelial corneal dystrophy.Cell death & disease · 2026Article
- Bimekizumab and progressive pulmonary fibrosis in severe psoriasis: a case report.Frontiers in medicine · 2026Article
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Immunotherapy-induced sialadenitis: sjögren's syndrome or a new sialadenitis.Frontiers in immunology · 2026Article
- A Narrative Review of Salivary Gland Extracellular Matrix and Sjögren's Syndrome: Research Status and Future Prospects.Biomolecules · 2026Review
- Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025Review
- Metformin Attenuates Partial Epithelial-Mesenchymal Transition in Salivary Gland Inflammation via PI3K/Akt/GSK3β/Snail Signaling Axis.Inflammation · 2025Article
- Th22 cells promote the transition from homeostatic to reactive microglia in diabetic encephalopathy.Acta diabetologica · 2025Article
- G protein-coupled receptor kinase 2 as a novel therapeutic target for gland fibrosis of Sjögren's syndrome.Acta pharmacologica Sinica · 2024Article
- Exploring Salivary Epithelial Dysfunction in Sjögren's Disease.International journal of molecular sciences · 2024Review
- Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2024Review
- Targeting Interleukin-17 as a Novel Treatment Option for Fibrotic Diseases.Journal of clinical medicine · 2023Review
- Interleukin-22 Inhibits Apoptosis of Gingival Epithelial Cells Through TGF-β Signaling Pathway During Periodontitis.Inflammation · 2023Article
- Involvement of Epithelial-Mesenchymal Transition (EMT) in Autoimmune Diseases.International journal of molecular sciences · 2023Review
- The Role of IL-17 in the Pathogenesis of Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2023Review
- Primary-Sjögren's-Syndrome-Related Interstitial Lung Disease: A Clinical Review Discussing Current Controversies.Journal of clinical medicine · 2023Review
- Anti-vimentin antibodies are associated with higher severity of Sjögren's disease.Clinical immunology (Orlando, Fla.) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary Sjögren's syndrome (pSS) is a chronic inflammatory, autoimmune and systemic disorder commonly associated with dry eyes and a dry mouth. Recently, the hypothetical link between epithelial-mesenchymal transition (EMT)-dependent salivary gland (SG) fibrosis and chronic inflammatory conditions has been suggested. In this study, we present data demonstrating a negative correlation of the epithelial marker E-cadherin expression and a positive correlation of mesenchymal vimentin and collagen type I expression with increasing degrees of tissue inflammation in pSS SG specimens. In addition, as it is not clear whether dysregulated cytokines in pSS, interleukin (IL)-17 and IL-22 may also contribute to the EMT-dependent fibrosis process, the effect of IL-17 and IL-22 treatment on EMT-dependent SG fibrosis was evaluated in primary human salivary gland epithelial cells (SGEC) isolated from healthy subjects. Here we present data demonstrating that IL-17 and IL-22 can induce SGEC to undergo a morphological and phenotypical transition to a mesenchymal phenotype. In support of this, vimentin and collagen type I were up-regulated while a decreased expression of E-cadherin occurs after interleukin treatment, and co-operation between IL-17 and Il-22 was required to induce the EMT.
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