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Journal of Immunology Research
Volume 2015, Article ID 979167, 8 pages
Review Article

Immune Disorders in Hashimoto’s Thyroiditis: What Do We Know So Far?

1Department of Endocrinology, Medical University, 20-059 Lublin, Poland
2Department of Immunology, Medical University, 20-059 Lublin, Poland

Received 16 January 2015; Revised 27 March 2015; Accepted 9 April 2015

Academic Editor: Xiao-Feng Yang

Copyright © 2015 Aleksandra Pyzik et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This review of literature attempts to identify the factors that are involved in the pathogenesis of Hashimoto thyroiditis, an immune defect in an individual with genetic susceptibility accompanied with environmental factors. The frequency of Hashimoto’s disease is a growing trend and among Caucasians it is estimated at approximately 5%. The dysfunction of the gland may be clinically evident (0.1–2% of the population) or subclinical (10–15%). The pathology is diagnosed five to ten times more often in women than men and its incidence increases with the age (the peak of the number of cases is between 45 and 65); however, it can also be diagnosed in children. The pathogenesis of Hashimoto’s thyroiditis is still not fully comprehended. In the etiology of Hashimoto thyroiditis excessively stimulated T CD4+ cells are known to play the most important role. Recent research has demonstrated an increasing role of newly discovered cells such as Th17 (CD4+IL-17+) or T regulatory cells (CD4+CD25FoxP3+) in the induction of autoimmune disorders. The process of programmed cell death also plays an equally important role in the pathogenesis and the development of hypothyroidism.