ArticleJournal of immunology (Baltimore, Md. : 1950)2015
A unique mouse strain that develops spontaneous, iodine-accelerated, pathogenic antibodies to the human thyrotrophin receptor.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Expression, immunogenicity and clinical significance analysis of thyroid‑stimulating hormone receptor fusion proteins.Molecular medicine reports · 2025Article
- The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 2022Review
- Is There Evidence for IGF1R-Stimulating Abs in Graves' Orbitopathy Pathogenesis?International journal of molecular sciences · 2020Review
- Graves' disease.Nature reviews. Disease primers · 2020Review
- Review
- A Mouse Thyrotropin Receptor A-Subunit Transgene Expressed in Thyroiditis-Prone Mice May Provide Insight into Why Graves' Disease Only Occurs in Humans.Thyroid : official journal of the American Thyroid Association · 2019Article
- Nanoparticles Bearing TSH Receptor Protein and a Tolerogenic Molecule Do Not Induce Immune Tolerance but Exacerbate Thyroid Autoimmunity in hTSHR/NOD.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- To reflect human autoimmune thyroiditis, thyroid peroxidase (not thyroglobulin) antibodies should be measured in female (not sex-independent) NOD.H2Clinical and experimental immunology · 2019Article
- Graves' orbitopathy occurs sex-independently in an autoimmune hyperthyroid mouse model.Scientific reports · 2018Article
- Thyroid Hemiagenesis in a Thyroiditis Prone Mouse Strain.European thyroid journal · 2018Article
- Gut microbiota in experimental murine model of Graves' orbitopathy established in different environments may modulate clinical presentation of disease.Microbiome · 2018Article
- Genetic immunization with mouse thyrotrophin hormone receptor plasmid breaks self-tolerance for a murine model of autoimmune thyroid disease and Graves' orbitopathy.Clinical and experimental immunology · 2018Article
- Aberrant Iodine Autoregulation Induces Hypothyroidism in a Mouse Strain in the Absence of Thyroid Autoimmunity.Journal of the Endocrine Society · 2018Article
- New advances in understanding thyroid-associated ophthalmopathy and the potential role for insulin-like growth factor-I receptor.F1000Research · 2018Review
- Variable Effects of Dietary Selenium in Mice That Spontaneously Develop a Spectrum of Thyroid Autoantibodies.Endocrinology · 2017Article
- High-level intrathymic thyrotrophin receptor expression in thyroiditis-prone mice protects against the spontaneous generation of pathogenic thyrotrophin receptor autoantibodies.Clinical and experimental immunology · 2017Article
- Genes Outside the Major Histocompatibility Complex Locus Are Linked to the Development of Thyroid Autoantibodies and Thyroiditis in NOD.H2h4 Mice.Endocrinology · 2017Article
- Thyroid Autoantibodies Display both "Original Antigenic Sin" and Epitope Spreading.Frontiers in immunology · 2017Review
- Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017Review
- Critical Differences between Induced and Spontaneous Mouse Models of Graves' Disease with Implications for Antigen-Specific Immunotherapy in Humans.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Abs that stimulate the thyrotropin receptor (TSHR), the cause of Graves' hyperthyroidism, only develop in humans. TSHR Abs can be induced in mice by immunization, but studying pathogenesis and therapeutic intervention requires a model without immunization. Spontaneous, iodine-accelerated, thyroid autoimmunity develops in NOD.H2(h4) mice associated with thyroglobulin and thyroid-peroxidase, but not TSHR, Abs. We hypothesized that transferring the human TSHR A-subunit to NOD.H2(h4) mice would result in loss of tolerance to this protein. BALB/c human TSHR A-subunit mice were bred to NOD.H2(h4) mice, and transgenic offspring were repeatedly backcrossed to NOD.H2(h4) mice. All offspring developed Abs to thyroglobulin and thyroid-peroxidase. However, only TSHR-transgenic NOD.H2(h4) mice (TSHR/NOD.H2(h4)) developed pathogenic TSHR Abs as detected using clinical Graves' disease assays. As in humans, TSHR/NOD.H2(h4) female mice were more prone than male mice to developing pathogenic TSHR Abs. Fortunately, in view of the confounding effect of excess thyroid hormone on immune responses, spontaneously arising pathogenic human TSHR Abs cross-react poorly with the mouse TSHR and do not cause thyrotoxicosis. In summary, the TSHR/NOD.H2(h4) mouse strain develops spontaneous, iodine-accelerated, pathogenic TSHR Abs in female mice, providing a unique model to investigate disease pathogenesis and test novel TSHR Ag-specific immunotherapies aimed at curing Graves' disease in humans.
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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.