ArticleClinical and experimental immunology2003
Dendritic cells infected with adenovirus expressing the thyrotrophin receptor induce Graves' hyperthyroidism in BALB/c mice.
Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
- Establishment and Comparison of Two Different Animal Models of Graves' Orbitopathy.Translational vision science & technology · 2023Article
- Antibodies against thyroid-stimulating hormone receptor cause maternal-neonatal transmission of Graves' Disease.Experimental and therapeutic medicine · 2021Article
- Quantitative Measurement of the Thyroid Uptake Function of Mouse by Cerenkov Luminescence Imaging.Scientific reports · 2017Article
- Review of Mouse Models of Graves' Disease and Orbitopathy-Novel Treatment by Induction of Tolerance.Clinical reviews in allergy & immunology · 2017Review
- TSH Receptor Cleavage Into Subunits and Shedding of the A-Subunit; A Molecular and Clinical Perspective.Endocrine reviews · 2016Review
- Withdrawn: TSH Receptor Cleavage Into Subunits and Shedding of the A-Subunit; A Molecular and Clinical Perspective.Endocrine reviews · 2016Review
- Excessive Cytosolic DNA Fragments as a Potential Trigger of Graves' Disease: An Encrypted Message Sent by Animal Models.Frontiers in endocrinology · 2016Review
- Evidence that TSH Receptor A-Subunit Multimers, Not Monomers, Drive Antibody Affinity Maturation in Graves' Disease.The Journal of clinical endocrinology and metabolism · 2015Article
- Breaking tolerance to thyroid antigens: changing concepts in thyroid autoimmunity.Endocrine reviews · 2014Review
- Delineating the autoimmune mechanisms in Graves' disease.Immunologic research · 2012Review
- Distribution of subpopulations of dendritic cells in peripheral blood of patients treated with exogenous thyrotropin.Thyroid research · 2012Article
- Attenuation of induced hyperthyroidism in mice by pretreatment with thyrotropin receptor protein: deviation of thyroid-stimulating to nonfunctional antibodies.Endocrinology · 2009Article
- Shared and unique susceptibility genes in a mouse model of Graves' disease determined in BXH and CXB recombinant inbred mice.Endocrinology · 2008Article
- Cancer immunotherapy using dendritic/tumour-fusion vaccine induces elevation of serum anti-nuclear antibody with better clinical responses.Clinical and experimental immunology · 2006Article
- Induction of hyperthyroidism in mice by intradermal immunization with DNA encoding the thyrotropin receptor.Clinical and experimental immunology · 2004Article
- Evidence that factors other than particular thyrotropin receptor T cell epitopes contribute to the development of hyperthyroidism in murine Graves' disease.Clinical and experimental immunology · 2004Article
- Thyrotrophin receptor-specific memory T cell responses require normal B cells in a murine model of Graves' disease.Clinical and experimental immunology · 2003Article
- Insight into antibody responses induced by plasmid or adenoviral vectors encoding thyroid peroxidase, a major thyroid autoantigen.Clinical and experimental immunology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic cells (DCs) are the most potent antigen-presenting cells and a prerequisite for the initiation of primary immune response. This study was performed to investigate the contribution of DCs to the initiation of Graves' hyperthyroidism, an organ-specific autoimmune disease in which the thyrotrophin receptor (TSHR) is the major autoantigen. DCs were prepared from bone marrow precursor cells of BALB/c mice by culturing with granulocyte macrophage-colony stimulating factor and interleukin-4. Subcutaneous injections of DCs infected with recombinant adenovirus expressing the TSHR (but not beta-galactosidase) in syngeneic female mice induced Graves'-like hyperthyroidism (8 and 35% of mice after two and three injections, respectively) characterized by stimulating TSHR antibodies, elevated serum thyroxine levels and diffuse hyperplasitc goiter. TSHR antibodies determined by ELISA were of both IgG1 (Th2-type) and IgG2a (Th1-type) subclasses, and splenocytes from immunized mice secreted interferon-gamma (a Th1 cytokine), not interleukin-4 (a Th2 cytokine), in response to TSHR antigen. Surprisingly, IFN-gamma secretion, and induction of antibodies and disease were almost completely suppressed by co-administration of alum/pertussis toxin, a Th2-dominant adjuvant, whereas polyriboinosinic polyribocytidylic acid, a Th1-inducer, enhanced splenocyte secretion of IFN-gamma without changing disease incidence. These observations demonstrate that DCs efficiently present the TSHR to naive T cells to induce TSHR antibodies and Graves'-like hyperthyroidism in mice. In addition, our results challenge the previous concept of Th2 dominance in Graves' hyperthyroidism and provide support for the role of Th1 immune response in disease pathogenesis.
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