Abstract

Hashimoto’s thyroiditis (HT) is the most prevalent autoimmune disorder of the thyroid (AITD) and characterized by the presence of circulating autoantibodies evoked by a, to date, not fully understood dysregulation of the immune system. Autoreactive lymphocytes and inflammatory processes in the thyroid gland can impair or enhance thyroid hormone secretion. MicroRNAs (miRNAs) are small noncoding RNAs, which can play a pivotal role in immune functions and the development of autoimmunity. The aim of the present study was to evaluate whether the expression of 9 selected miRNAs related to immunological functions differ in patients with HT compared to healthy controls. MiRNA profiles were analysed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) in 24 patients with HT and 17 healthy controls. Systemic expressions of miR-21-5p, miR-22-3p, miR-22-5p, miR-142-3p, miR-146a-5p, miR-301-3p and miR-451 were significantly upregulated in patients with HT (p ≤ 0.01) and were suitable to discriminate between HT and healthy controls in AUC analysis. Altered expressions of miR-22-5p and miR-142-3p were associated with higher levels of thyroid antibodies, suggesting their contribution to the pathogenesis of HT.

Highlights

  • Autoimmune thyroid diseases (AITDs) are the most common autoimmune diseases, affecting 2–5% of the population in high-income countries [1]

  • This observational trial was initiated in the year 2010 and the study population consists of 1022 asymptomatic subjects without diagnosed cardiovascular disease (CVD) with at least one classical risk factor for CVD, such as family history of CVD, hypertension or dyslipidaemia

  • In the present observational study, eight out of nine observed miRNAs were differentially expressed in the serum of Hashimoto’s thyroiditis (HT) patients compared to healthy controls

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Summary

Introduction

Autoimmune thyroid diseases (AITDs) are the most common autoimmune diseases, affecting 2–5% of the population in high-income countries [1]. Hashimoto’s thyroiditis (HT), the most frequent AITD, is the leading cause of hypothyroidism in iodine-sufficient areas of the world. Exact mechanisms of aetiology and pathogenesis of HT are not completely understood, a strong genetic susceptibility to the disease has been confirmed by studies carried out within families and twins [2]. As in other autoimmune disorders, humoral and cellular immune mechanisms are closely related and cross-linked in AITDs. Disturbed self-tolerance accompanied by an increased antigen presentation is a precondition for their manifestation, based on the interaction of thyroid, antigen presenting and T cells. Secreted cytokines provoke predominantly a T-helper type 1 (Th1)

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