Arpaci Dilek, Karakas Celik Sevim, Can Murat, Cakmak Genc Gunes, Kuzu Fatih, Unal Mustafa, Bayraktaroglu Taner
a Bulent Ecevit University , Faculty of Medicine, Department of Endocrinology and Metabolism , Zonguldak , Turkey.
b Bulent Ecevit University , Faculty of Sciences and Arts, Department of Molecular Biology and Genetics , Zonguldak Turkey.
Immunol Invest. 2016 Oct;45(7):668-78. doi: 10.1080/08820139.2016.1208215. Epub 2016 Sep 12.
Hashimoto's thyroiditis (HT) is thought to result from decreased T helper type 2 (Th2) responses, leading to the progressive destruction of thyrocytes. IFN-λ1, -λ2, and -λ3 (also known as IL-29, IL-28A, and IL-28B, respectively) are recently described members of the IFN-λ family and have been shown to decrease the production of Th2 cytokines in vitro. However, the role and mechanism of IFN-λ1 in HT remain unknown. The purpose of this study was to examine whether IL29 and IL28B gene polymorphisms are susceptibility genes for the development of HT. Also, we investigated the effects of IL-29 and IL-28 serum levels in the pathogenesis of HT. Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, single-nucleotide polymorphisms (SNPs) of IL28B rs8099917 (IL28 G/T) and IL29 rs30461 (IL29 T/C) were studied in 99 patients with HT and 100 healthy controls. Considering the allelic distribution of the IL28 G/T polymorphism, a higher frequency of the G allele was observed in the control group versus the HT group. Thus, it was suggested that the G allele may be protective against HT pathogenesis (OR = 0.388, 95% CI = 0.217-0.693; p = 0.001). Our findings also demonstrated that there was a statistically significant difference in serum IL-28 and IL-29 levels between case and control groups (p < 0.001). Increased serum levels of IL-28 and IL-29 were found in patients with HT. However, we did not find a relationship between the IL29 gene polymorphism and HT. In conclusion, the IL28B gene polymorphism and serum IL-28 and IL-29 levels seem to play a role in the pathogenesis of HT.
桥本甲状腺炎（HT）被认为是由2型辅助性T细胞（Th2）反应降低所致，进而导致甲状腺细胞的渐进性破坏。干扰素λ1、λ2和λ3（也分别称为IL-29、IL-28A和IL-28B）是最近被描述的干扰素λ家族成员，并且已显示在体外可降低Th2细胞因子的产生。然而，干扰素λ1在HT中的作用和机制仍不清楚。本研究的目的是检查IL29和IL28B基因多态性是否为HT发生发展的易感基因。此外，我们还研究了IL-29和IL-28血清水平在HT发病机制中的作用。采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）方法，对99例HT患者和100名健康对照者的IL28B rs8099917（IL28 G/T）和IL29 rs30461（IL29 T/C）单核苷酸多态性（SNP）进行了研究。考虑到IL28 G/T多态性的等位基因分布，与HT组相比，在对照组中观察到G等位基因的频率更高。因此，提示G等位基因可能对HT发病机制具有保护作用（OR = 0.388，95%CI = 0.217 - 0.693；p = 0.001）。我们的研究结果还表明，病例组和对照组之间血清IL-28和IL-29水平存在统计学显著差异（p < 0.001）。在HT患者中发现血清IL-28和IL-29水平升高。然而，我们未发现IL29基因多态性与HT之间存在关联。总之，IL28B基因多态性以及血清IL-28和IL-29水平似乎在HT发病机制中发挥作用。
