ArticleThe Journal of endocrinology2011
Orbital fibrosis in a mouse model of Graves' disease induced by genetic immunization of thyrotropin receptor cDNA.
Article in The Journal of endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 79 citations in OpenAlex.
- Maraviroc attenuates orbital remodeling, inflammation, and lipid dysregulation in a murine model of thyroid eye disease associated with Graves' disease.Frontiers in endocrinology · 2026Article
- How to manage thyroid eye disease: recent advances - a narrative review.Drugs in context · 2026Review
- PDGFRαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeted Delivery of CD34 Aptamer-Coupled Tocilizumab Microspheres for Effective Treatment of Thyroid-Associated Ophthalmopathy.Investigative ophthalmology & visual science · 2025Article
- The miR-320a/PRDX3 Axis Alleviates the Oxidative Stress and Fibrotic Alterations in Fibroblasts in Thyroid Eye Disease.Investigative ophthalmology & visual science · 2025Article
- Butyrate Ameliorates Graves' Orbitopathy Through Regulating Orbital Fibroblast Phenotypes and Gut Microbiota.Investigative ophthalmology & visual science · 2025Article
- Mouse model of Graves' orbitopathy induced by the immunization with TSHR A and IGF-1R α subunit gene.Journal of endocrinological investigation · 2024Article
- Impact of ibrutinib on inflammation in a mouse model of Graves' orbitopathy.Frontiers in endocrinology · 2024Article
- Establishment and Comparison of Two Different Animal Models of Graves' Orbitopathy.Translational vision science & technology · 2023Article
- A review of TSHR- and IGF-1R-related pathogenesis and treatment of Graves' orbitopathy.Frontiers in immunology · 2023Review
- TGFβ-Treated Placenta-Derived Mesenchymal Stem Cells Selectively Promote Anti-Adipogenesis in Thyroid-Associated Ophthalmopathy.International journal of molecular sciences · 2022Article
- 2021 update on thyroid-associated ophthalmopathy.Journal of endocrinological investigation · 2022Review
- MiR-143 Targets IGF-1R to Suppress Autoimmunity in Thyroid-Associated Ophthalmopathy.Journal of inflammation research · 2022Article
- Expression of Endogenous Putative TSH Binding Protein in Orbit.Current issues in molecular biology · 2021Article
- Orbital Signaling in Graves' Orbitopathy.Frontiers in endocrinology · 2021Review
- The Role of the Microbiota in Graves' Disease and Graves' Orbitopathy.Frontiers in cellular and infection microbiology · 2021Review
- Tissue block staining and domestic adhesive tape yield qualified integral sections of adult mouse orbits and eyeballs.PloS one · 2021Article
- Microbiome and Graves' Orbitopathy.European thyroid journal · 2020Article
- A Novel Long-Term Graves' Disease Animal Model Confirmed by Functional Thyrotropin Receptor Antibodies.European thyroid journal · 2020Article
- Graves' disease.Nature reviews. Disease primers · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The TSH receptor (TSHR) is the critical target for antibody production in Graves' disease (GD). Insulin-like growth factor 1 receptor (IGF1R) has been proposed as a second autoantigen in complications of GD such as orbitopathy. We attempted to induce orbital tissue remodeling in mice undergoing immunizations with plasmids encoding TSHR and IGF1R delivered by in vivo skeletal muscle electroporation, a procedure known to give a sustained, long-term antibody response. Female BALB/c mice were challenged with TSHR A-subunit or IGF1Rα subunit plasmid by injection and electroporation. Mice challenged with TSHR A-subunit plasmid resulted in high frequency (75%) of hyperthyroidism and thyroid-stimulating antibodies. But strikingly, immunization with TSHR A-subunit plasmid also elicited antibody to IGF1Rα subunit. Mice challenged in the same manner with IGF1Rα subunit plasmid produced strong antibody responses to IGF1R, but did not undergo any changes in phenotype. Simultaneous challenge by double antigen immunization with the two plasmids in distant anatomical sites reduced the incidence of hyperthyroidism, potentially as a consequence of antigenic competition. Thyroid glands from the TSHR A-subunit plasmid-challenged group were enlarged with patchy microscopic infiltrates. Histological analysis of the orbital tissues demonstrated moderate connective tissue fibrosis and deposition of Masson's trichrome staining material. Our findings imply that immunization with TSHR A-subunit plasmid leads to generation of IGF1R antibodies, which together with thyroid-stimulating antibodies may precipitate remodeling of orbital tissue, raising our understanding of its close association with GD.
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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.