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Pathogenesis

Pathogenesis

Copyright: © 2020 |Pages: 40
ISBN13: 9781522596554|ISBN10: 1522596550|ISBN13 Softcover: 9781522596561|EISBN13: 9781522596578
DOI: 10.4018/978-1-5225-9655-4.ch006
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MLA

Mahmoud Sakr. "Pathogenesis." Diagnosing and Managing Hashimoto’s Disease: Emerging Research and Opportunities, IGI Global, 2020, pp.48-87. https://doi.org/10.4018/978-1-5225-9655-4.ch006

APA

M. Sakr (2020). Pathogenesis. IGI Global. https://doi.org/10.4018/978-1-5225-9655-4.ch006

Chicago

Mahmoud Sakr. "Pathogenesis." In Diagnosing and Managing Hashimoto’s Disease: Emerging Research and Opportunities. Hershey, PA: IGI Global, 2020. https://doi.org/10.4018/978-1-5225-9655-4.ch006

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Abstract

Hashimoto's thyroiditis (HT) is one of the most prevalent autoimmune diseases provoked in genetically susceptible individuals by several triggers. Immune-regulatory genes such as HLA, CTLA-4, and PTPN22 play a major role in the pathogenesis of autoimmune thyroiditis. The thyroid-specific gene currently showing the association with HT (and also Graves' disease) is the gene for thyroglobulin (Tg). The VDR gene is another HT predisposing gene, common for other organ-specific autoimmune diseases such as type-I diabetes or Addison's disease. Furthermore, cytokine genes such as IFN-γ, IL-4, or TGF-β indicate the association with the development and severity of HT. A complex interaction between genetic and non-genetic factors results in enhanced thyroid antigen presentation and reduced immune tolerance leading to predominantly Th1-type autoimmunity, thyroid destruction, and clinical disease. The exact mechanisms of initiation and progression of HT are yet to be clarified. This chapter explores the pathogenesis of Hashimoto's disease.

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