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Mediators of Inflammation
Volume 2017 (2017), Article ID 3916395, 8 pages
Review Article

General and Specific Genetic Polymorphism of Cytokines-Related Gene in AITD

1Department of General Surgery, Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing, China
2State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, Beijing, China
3Department of Medical Service, The Third Clinical Medical College, Beijing University of Chinese Medicine, Beijing, China

Correspondence should be addressed to Ding Zhiguo

Received 14 October 2016; Revised 4 December 2016; Accepted 12 December 2016; Published 4 January 2017

Academic Editor: Jun-hui Wang

Copyright © 2017 Chen Xiaoheng 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.


Autoimmune thyroid disease (AITD) shows the highest incidence among organ-specific autoimmune diseases and is the most common thyroid disease in humans, including Graves’ disease (GD) and Hashimoto’s thyroiditis (HT). The susceptibility to autoimmune diseases is affected by increased autoantibody levels, susceptibility gene polymorphisms, environmental factors, and psychological factors, but the pathogenesis remains unclear. Various cytokines and related genes encoding them play important roles in the development and progression of AITD. CD152, an expression product of the CTLA-4 gene, downregulates T cell activation. The A/A genotype polymorphism in the CT60 locus may reduce the production of thyroid autoantibodies. The C1858T polymorphism of the PTNP22 gene reduces the expression of its encoded LYP, which increases the risk of GD and HT. GD is an organ-specific autoimmune disease involving increased secretion of thyroid hormone, whereas HT may be associated with the destruction of thyroid gland tissue and hypothyroidism. These two diseases exhibit similar pathogenesis but opposite trends in the clinical manifestations. In this review, we focus on the structure and function of these cytokines and related genes in AITD, as well as the association of polymorphisms with susceptibility to GD and HT, and attempt to describe their differences in pathogenesis and clinical manifestations.