ArticleJournal of endocrinological investigation2017
Low regulatory T cell and high IL-17 mRNA expression in a mouse Graves' disease model.
Article in Journal of endocrinological investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Expression levels of T cell-related immune factors and their correlation with thyroid function in Graves' disease with varied serum iodine status: insights into immunopathogenesis.Frontiers in endocrinology · 2025Article
- Immune tolerance induction using the thyrotropin receptor epitope 78-94 (p37) prevents Graves' disease in HLA-DR3 transgenic mice.Frontiers in immunology · 2025Article
- Alcohol-induced bone loss driven by dysregulated spatial distribution of gut microbiota and PGD2-IL17 pathway-mediated osteoclast activation.Frontiers in microbiology · 2025Article
- Article
- Unveiling the Role of Gut Microbiota and Metabolites in Autoimmune Thyroid Diseases: Emerging Perspectives.International journal of molecular sciences · 2024Review
- Evaluating the causal effects between Grave's disease and diabetes mellitus: a bidirectional Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Effect of methimazole treatment on Th1, Th17, and Th22 lymphocytes in pediatric Graves' disease patients.Frontiers in immunology · 2024Article
- Th17 cytokines and factors modulating their activity in patients with pernicious anemia.Immunologic research · 2023Article
- Fibrocyte Participation in Thyroid-Associated Ophthalmopathy Suggests New Approaches to Therapy.Ophthalmic plastic and reconstructive surgery · 2023Review
- Regulatory T Cells in the Pathogenesis of Graves' Disease.International journal of molecular sciences · 2023Review
- [The features of regulatory T-blood cells subpopulation and the level of CD25 expression in patients with Graves' disease in dynamics after radioactive iodine therapy].Problemy endokrinologii · 2023Article
- A Global Regulatory Network for Dysregulated Gene Expression and Abnormal Metabolic Signaling in Immune Cells in the Microenvironment of Graves' Disease and Hashimoto's Thyroiditis.Frontiers in immunology · 2022Article
- Saikosaponin-d Attenuates Hashimoto's Thyroiditis by Regulating Macrophage Polarization.Journal of immunology research · 2022Article
- Changes in Th9 and Th17 lymphocytes and functional cytokines and their relationship with thyroid-stimulating hormone receptor antibodies at different stages of graves' disease.Frontiers in immunology · 2022Article
- Gut Microbiome and the Role of Metabolites in the Study of Graves' Disease.Frontiers in molecular biosciences · 2022Review
- Decreased Treg Cell and TCR Expansion Are Involved in Long-Lasting Graves' Disease.Frontiers in endocrinology · 2021Article
- Genetics, Epigenetics, Cellular Immunology, and Gut Microbiota: Emerging Links With Graves' Disease.Frontiers in cell and developmental biology · 2021Review
- Insulin-like Growth Factor-I Receptor and Thyroid-Associated Ophthalmopathy.Endocrine reviews · 2019Review
- Elevated Serum IL-17 Expression at Cessation Associated with Graves' Disease Relapse.International journal of endocrinology · 2018Article
- The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGraves' disease (GD) is an autoimmune thyroid disease, and the most important characteristic of it is the presence of the thyroid-stimulating antibody (TSAb). The mechanisms of the TSAb elevation are still uncertain. Recent studies have suggested that the dysregulation of regulatory T cell (Treg) and T helper 17 (Th17) might stimulate the production of TSAb and be a pathogenesis of GD. However, the role of Treg and Th17 cells in the pathogenesis of GD is still debated. Our aim is to assess changes of Treg and Th17 cells in the spleen of a mouse in an in vivo GD model and try to explain the pathogenesis of GD.
methodsWe used an adenovirus expressing the autoantigen thyroid-stimulating hormone receptor (Ad-TSHR289) to immunise mice in order to induce GD in the model. Flow cytometry was used to measure the frequencies of splenic Treg and Th17 cells and real-time PCR to analyse the mRNA expression of forkhead box P3(Foxp3) and interleukin-17(IL-17).
resultsCompared with the Ad-Control group, the frequencies of CD4
conclusionsThe pathogenesis of GD may be associated with reduced Treg cells and increased IL-17 gene expression. The increased IL-17 mRNA needs to be explained by other mechanisms but not Th17 cells.
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