ArticleJournal of translational medicine2020
Metabolic abnormalities exacerbate Sjögren's syndrome by and is associated with increased the population of interleukin-17-producing cells in NOD/ShiLtJ mice.
Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Therapeutic effects of a synthetic glabridin derivative on metabolic immuno-regulation and salivary gland functional restoration in experimental Sjögren's syndrome.Experimental & molecular medicine · 2026Article
- Exosomes derived from stem cells from apical papilla reduce Th17 cell differentiation and hyposalivation in a murine model of Sjögren's disease.BMC oral health · 2026Article
- Genetic Crosstalk Between Type 1 Diabetes and Sjögren's Syndrome: A Systematic Exploration of Risk Genes and Common Pathways.Journal of cellular and molecular medicine · 2025Article
- Pharmacological Mechanisms of CheReCunJin Formula in Ameliorating Sjögren's Syndrome: Suppression of IL-17 Signal-Mediated Inflammatory Cascade.Journal of inflammation research · 2025Article
- Pathogenesis and treatment of Sjogren's syndrome: Review and update.Frontiers in immunology · 2023Review
- TLR7 agonism accelerates disease in a mouse model of primary Sjögren's syndrome and drives expansion of T-betFrontiers in immunology · 2022Article
- Association Between Endometriosis and Subsequent Risk of Sjögren's Syndrome: A Nationwide Population-Based Cohort Study.Frontiers in immunology · 2022Article
- Sexual dimorphism in immunometabolism and autoimmunity: Impact on personalized medicine.Autoimmunity reviews · 2021Review
- IL-17 and CCR9Frontiers in immunology · 2021Article
- IL-17 in pancreatic disease: pathogenesis and pharmacotherapy.American journal of cancer research · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSjögren's syndrome (SS) is an autoimmune disease mediated by lymphocytic infiltration into exocrine glands, resulting in progressive lacrimal and salivary destruction and dysfunctional glandular secretion. Metabolic syndrome influences the immune system. To investigate its relationship with metabolic abnormalities, we evaluated the pathogenesis of SS and the immune cell populations in non-obese diabetic NOD/ShiLtJ mice with type 1 diabetes (T1D).
methodsTo induce metabolic abnormalities, streptozotocin (STZ)-a glucosamine-nitrosourea compound that destroys pancreatic β cells, resulting in T1D-was injected into NOD/ShiLtJ mice. The blood glucose level was measured to evaluate induction of T1D. The severity of SS was assessed by determining the body weight, salivary flow rate, and histologic parameters. The expression levels of proinflammatory factors in the salivary glands, lacrimal gland, and spleen were quantified by real-time PCR. The populations of various T- and B-cell subtypes in the peripheral blood, spleen, and salivary glands were assessed by flow cytometry.
resultsInduction of T1D in NOD/ShiLtJ mice increased both the severity of SS and the levels of proinflammatory cytokines in the salivary glands compared to the controls. Furthermore, the number of interleukin-17-producing immune cells in the peripheral blood, spleen, and salivary glands was increased in STZ- compared to vehicle-treated NOD/ShiLtJ mice.
conclusionsMetabolic abnormalities play an important role in the development of SS.
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