ArticleJournal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology2013
Salivary gland hypofunction induced by activation of innate immunity is dependent on type I interferon signaling.
Article in Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Biosemantics guided gene expression profiling of Sjögren's syndrome: a comparative analysis with systemic lupus erythematosus and rheumatoid arthritis.Arthritis research & therapy · 2017Pooled it
- Akt Signaling Pathway Is Activated in the Minor Salivary Glands of Patients with Primary Sjögren's Syndrome.International journal of molecular sciences · 2021Trial
- Molecular classification of primary Sjögren's syndrome based on salivary gland omics.Arthritis research & therapy · 2026Article
- Molecular Insights into Oral Manifestations in Sjögren's Disease.International journal of molecular sciences · 2026Review
- Maternal antibodies regulate the establishment of murine oral and salivary mucosal immunity.Nature communications · 2026Article
- The 'target tissues' as orchestrators of autoimmune responses: the paradigm of Sjögren's syndrome.Clinical and experimental immunology · 2026Review
- Investigating the role of tripartite motif containing-21 and interleukin-6 in pro-Inflammatory symptom-associated heterogeneity within primary Sjögren's syndrome.Rheumatology and immunology research · 2025Article
- Toll-like receptor 3: a double-edged sword.Biomarker research · 2025Review
- Endogenous IL-22 contributes to the pathogenesis of salivary gland dysfunction in the non-obese diabetic model of Sjögren's syndrome.Molecular immunology · 2024Article
- Amplified Type I Interferon Response in Sjögren's Disease via Ectopic Toll-Like Receptor 7 Expression in Salivary Gland Epithelial Cells Induced by Lysosome-Associated Membrane Protein 3.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- MICa/b-dependent activation of natural killer cells by CD64The EMBO journal · 2023Article
- Inhibition of NLRP3 inflammasome activity by MCC950 leads to exacerbation of Sjӧgren's syndrome pathologies in non-obese diabetic mice.Immunology · 2023Article
- Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2021Review
- The Role of Interferons in the Pathogenesis of Sjögren's Syndrome and Future Therapeutic Perspectives.Biomolecules · 2021Review
- Protocols for Experimental Sjögren's Syndrome.Current protocols in immunology · 2020Article
- The NZB/W F1 mouse model for Sjögren's syndrome: A historical perspective and lessons learned.Autoimmunity reviews · 2020Review
- Innate Immunity and Biological Therapies for the Treatment of Sjögren's Syndrome.International journal of molecular sciences · 2020Review
- Pulmonary Involvement in a Mouse Model of Sjögren's Syndrome Induced by STING Activation.International journal of molecular sciences · 2020Article
- Agonist-induced 4-1BB activation prevents the development of Sjӧgren's syndrome-like sialadenitis in non-obese diabetic mice.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Activation of Myd88-Dependent TLRs Mediates Local and Systemic Inflammation in a Mouse Model of Primary Sjögren's Syndrome.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundActivation of innate immunity through polyinosinic:polycytidylic acid [poly(I:C)] causes acute salivary gland hypofunction. As a major consequence of poly(I:C) treatment is type I interferon (IFN) production, this study was undertaken to investigate their role in salivary gland dysfunction.
methodsDifferent strains of mice deficient in either interferon alpha receptor (IFNAR1(-/-)) or IL-6(-/-), or IL-10(-/-), or EBI3(-/-) were treated with poly(I:C). Salivary gland function was determined by measuring pilocarpine-induced saliva volume. Gene expression levels were measured by real-time PCR. Ca(2+) mobilization studies were performed using ex-vivo acinar cells.
resultsA single injection of poly(I:C) rapidly induced salivary gland hypofunction in wild-type B6 mice (41% drop in saliva volumes compared to PBS-treated mice). In contrast, the loss of function in poly(I:C)-treated IFNAR(-/-) mice was only 9.6%. Gene expression analysis showed reduced levels of Il-6, Il-10, and Il-27 in submandibular glands of poly(I:C)-treated IFNAR(-/-) mice. While salivary gland dysfunction in poly(I:C)-treated IL-10(-/-) and EBI3(-/-) mice was comparable to wild-type mice, the IL-6(-/-) mice were more resistant, with only a 21% drop in function. Pilocarpine-induced Ca(2+) flux was significantly suppressed in acinar cells obtained from poly(I:C)-treated wild-type mice.
conclusionsOur data demonstrate that a combined action of type I IFNs and IL-6 contributes toward salivary gland hypofunction. This happens through interference with Ca(2+) mobilization within acinar cells. Thus, in acute viral infections and diseases like Sjögren's syndrome, elevated levels of type I IFNs and IL-6 can directly affect glandular function.
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