The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Autoimmune thyroid disorders
Open accessAbstract
Autoimmune thyroid diseases (AITD) result from a dysregulation of the immune system leading to an immune attack on the thyroid. AITD are T cell-mediated organ-specific autoimmune disorders. The prevalence of AITD is estimated to be 5%; however, the prevalence of antithyroid antibodies may be even higher. The AITD comprise two main clinical presentations: Graves' disease (GD) and Hashimoto's thyroiditis (HT), both characterized by lymphocytic infiltration of the thyroid parenchyma. The clinical hallmarks of GD and HT are thyrotoxicosis and hypothyroidism, respectively. The mechanisms that trigger the autoimmune attack to the thyroid are still under investigation. Epidemiological data suggest an interaction among genetic susceptibility and environmental triggers as the key factor leading to the breakdown of tolerance and the development of disease. Recent studies have shown the importance of cytokines and chemokines in the pathogenesis of AT and GD. In thyroid tissue, recruited T helper 1 (Th1) lymphocytes may be responsible for enhanced IFN-γ and TNF-α production, which in turn stimulates CXCL10 (the prototype of the IFN-γ-inducible Th1 chemokines) secretion from the thyroid cells, therefore creating an amplification feedback loop, initiating and perpetuating the autoimmune process. Associations exist between AITD and other organ specific (polyglandular autoimmune syndromes), or systemic autoimmune disorders (Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, cryoglobulinemia, sarcoidosis, psoriatic arthritis). Moreover, several studies have shown an association of AITD and papillary thyroid cancer. These data suggest that AITD patients should be accurately monitored for thyroid dysfunctions, the appearance of thyroid nodules, and other autoimmune disorders.
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Cites
Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease
Ueda, H., Howson, J. M. M., Esposito, L., Heward, J., Snook, Chamberlain, G., Rainbow, D. B., Hunter, K. M. D., Smith, A. N., Di Genova, G., et al. (2003) · Nature · doi:10.1038/nature01621 · Cited by 2,175
Epidemiology and estimated population burden of selected autoimmune diseases in the United States
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Chemokine (C–X–C motif) ligand (CXCL)10 in autoimmune diseases
Antonelli, A., Ferrari, S. M., Giuggioli, D., Ferrannini, E., Ferri, C., & Fallahi, P. (2014) · Autoimmunity Reviews · doi:10.1016/j.autrev.2013.10.010 · Cited by 595
Self-citationThe HLA Region and Autoimmune Disease: Associations and Mechanisms of Action
Simmonds, M., & Gough, S. (2007) · Current Genomics · doi:10.2174/138920207783591690 · Cited by 472
Polyglandular Autoimmune Syndromes: Immunogenetics and Long-Term Follow-Up
Dittmar, M., & Kahaly, G. J. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2002-021845 · Cited by 367
The incidence of autoimmune thyroid disease: a systematic review of the literature
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Cited by
Hashimotos' thyroiditis: epidemiology, pathogenesis, clinic and therapy
Ragusa, F., Fallahi, P., Elia, G., Gonnella, D., Paparo, S. R., Giusti, C., Churilov, L. P., Ferrari, S. M., & Antonelli, A. (2019) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2019.101367 · Cited by 655
Self-citationMolecular mimicry and autoimmunity
Rojas, M., Restrepo-Jiménez, P., Monsalve, D. M., Pacheco, Y., Acosta-Ampudia, Y., Ramírez-Santana, C., Leung, P. S. C., Ansari, A. A., Gershwin, M. E., & Anaya, J.-M. (2018) · Journal of Autoimmunity · doi:10.1016/j.jaut.2018.10.012 · Cited by 627
Ralli, M., Angeletti, D., Fiore, M., D'Aguanno, V., Lambiase, A., Artico, M., de Vincentiis, M., & Greco, A. (2020) · Autoimmunity Reviews · doi:10.1016/j.autrev.2020.102649 · Cited by 600
Immunogenetics of autoimmune thyroid diseases: a comprehensive review
Lee, H. J., Li, C. W., Hammerstad, S. S., Stefan, M., & Tomer, Y. (2015) · Journal of Autoimmunity · doi:10.1016/j.jaut.2015.07.009 · Cited by 351
IL-15 functions as a danger signal to regulate tissue-resident T cells and tissue destruction
Jabri, B., & Abadie, V. (2015) · Nature Reviews Immunology · doi:10.1038/nri3919 · Cited by 315
Metadata
- Authors
- Antonelli, A., Ferrari, S. M., Corrado, A., Di Domenicantonio, A., & Fallahi, P.
- Venue
- Autoimmunity Reviews
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 14
- Issue
- 2
- Pages
- 174-180
- ISSN
- 1568-9972 (ISSN-L)
- OpenAlex
- W2009484486
- Cited by
- 925
- References
- 10
- FWCI
- 29.92
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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