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Takashi Nanba, Mikio Watanabe, Takashi Akamizu, Yoshinori Iwatani, The −590CC Genotype in the IL4 Gene as a Strong Predictive Factor for the Development of Hypothyroidism in Hashimoto Disease, Clinical Chemistry, Volume 54, Issue 3, 1 March 2008, Pages 621–623, https://doi.org/10.1373/clinchem.2007.099739
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To the Editor:
The severity of Hashimoto disease (HD) varies among patients and is difficult to predict when the disease is in the subclinical state and diagnosed by the presence of thyroid-specific autoantibody. Likewise, the intractability of Graves disease (GD) is difficult to predict. Autoimmune thyroid destruction that underlies both diseases is strongly determined by T-cell cytotoxicity, which is activated by interferon (IFN)-γ (1), and the T allele in +874A/T polymorphism of the interferon gamma (IFNG) gene, which promotes increased IFN-γ production, has been noted more frequently among patients with severe HD (2). Cytokine balance between T-helper 1 (Th1) cytokines, such as IFN-γ, and Th2 cytokines is important in immune regulation (3). Therefore, it is possible that Th2 cytokines may also affect the severity of HD and the intractability of GD. Interleukin (IL)-4, one of the key Th2 cytokines, stimulates humoral immunity and suppresses the production of inflammatory Th1 cytokines, including IFN-γ (3). Individuals who carry the T allele in −590C/T polymorphism of the interleukin 4 (IL4) gene (rs2243250) have a higher proportion of IL-4–producing T-helper cells (4). Individuals with the Ile/Ile genotype in the Ile50Val polymorphism (rs1805010) of the interleukin 4 receptor, alpha (IL4RA) gene also have higher IL-4Rα activity compared to individuals with the Ile/Val or Val/Val genotype (5).
