Increased Serum Levels of IL-28 and IL-29 and Protective Effect of IL28B rs8099917 Polymorphism in Patients with Hashimoto

Dilek Arpaci; Sevim Karakas Celik; Murat Can; Cakmak Gunes; Fatih Kuzu; Mustafa Unal; Taner Bayraktaroglu

doi:10.1530/endoabs.41.EP989

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Endocrine Abstracts (2016) 41 EP989 | DOI: 10.1530/endoabs.41.EP989

ECE2016 Eposter Presentations Thyroid (non-cancer) (120 abstracts)

Increased Serum Levels of IL-28 and IL-29 and Protective Effect of IL28B rs8099917 Polymorphism in Patients with Hashimoto’s Thyroiditis

Dilek Arpaci ¹ , Sevim Karakas Celik ² , Murat Can ³ , Gunes Cakmak Gunes ⁴ , Fatih Kuzu ¹ , Mustafa Unal ¹ & Taner Bayraktaroglu ¹

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¹Bulent Ecevit University, Faculty of Medicine, Department of Endocrinology and Metabolism, Zonguldak, Turkey; ²Bulent Ecevit University, Faculty of Sciences and Arts, Department of Molecular Biology and Genetics, Zonguldak, Turkey; ³Bulent Ecevit University, Faculty of Medicine, Department of Biochemistry, Zonguldak, Turkey; ⁴Bulent Ecevit University, Faculty of Medicine, Department of Genetics, Zonguldak, Turkey.

Hashimoto’s thyroiditis is thought to result from the decreased of T helper type 2 (Th2) responses, leading to progressive destruction of thyrocytes. IFN-λ1, -λ2, and -λ3 (also known as IL-29, IL-28A, and IL-28B, respectively) is a recently described member of the IFN-λ family and has been shown to decrease production of Th2 cytokines in vitro. However, the role and mechanism of IFN-λ1 in Hashimoto’s thyroiditis remain unknown. The purpose of our study is to elucidate whether the IL-29 and IL-28B gene polymorphisms are susceptibility genes for the development of HT. Also we aimed to investigate the effects of IL-29 and IL-28 serum levels on pathogenesis of HT. Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, the 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 for IL28 G/T polymorphism a higher frequency of G allele was observed in the control group when compared to the HT group. So it was suggested that G allele may be a protective role for HT pathogenesis (OR=0.388 95%-CI 0.217-0.693; P=0.001). Also our findings demonstrate that there was statistically significant difference in serum IL-28 and IL-29 levels between case and control groups (P<0.001). The increased serum levels of IL-28 and IL-29 in patients with HT was determined. In conclusion, IL-28B gene polymorphism and serum IL-28 and IL-29 levels seemed to play a role in the pathogenesis of HT.