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桥本甲状腺炎患者血清白细胞介素-23和白细胞介素-17水平

SERUM LEVELS OF INTERLEUKIN - 23 AND INTERLEUKIN - 17 IN HASHIMOTO'S THYROIDITIS.

作者信息

Gerenova J, Manolova I, Stanilova S

机构信息

Trakia University, Medical Faculty, Dept. of Propeudetics of Internal Diseases, Stara Zagora, Bulgaria.

University Hospital - Endocrinology, Stara Zagora, Bulgaria.

出版信息

Acta Endocrinol (Buchar). 2019 Jan-Mar;-5(1):74-79. doi: 10.4183/aeb.2019.74.

Abstract

CONTEXT

Overproduction of proinflammatory cytokines plays a significant role in the pathogenesis of Hashimoto's thyroiditis (HT). Recent studies revealed a prominent role of newly discovered Th17 subset in the induction of autoimmune disorders and that the signaling induced by IL-23 on Th17 cells is crucial to obtain a pathogenic and sustained phenotype. The objective of this study was to provide the involvement of interleukin IL-23/IL-17 axis in pathologic processes.

DESIGN

Serum levels of IL-23 and IL-17 in controls and HT patients were studied in different stages of disease activity.

SUBJECTS AND METHODS

We investigated 93 patients with HT: 33 patients with newly diagnosed euthyroid HT (Group I), 11 patients with newly diagnosed hypothyroid HT (Group II), and 49 subjects treated with Levothyroxine (Group III). Thirty healthy subjects were included as controls. Concentrations of IL-23 and IL-17 in the serum samples of patients and controls were evaluated by enzyme-linked immunosorbent assay.

RESULTS

Serum level of IL-23 was significantly higher in all HT patients (p<0.0001) as well as in subgroups of patients in comparison with controls (p<0.01). Serum concentrations of IL-17 were statistically increased in the group of HT patients (p=0.014); the differences in IL-17 levels between groups I and III in comparison to healthy controls were also significant, but not for group II.

CONCLUSIONS

Our results highlight the involvement of the IL-23/IL-17 axis in the development of HT and its severity. Moreover, upregulated secretion of IL-23 could be a biomarker for progression and monitoring of HT.

摘要

背景

促炎细胞因子的过度产生在桥本甲状腺炎(HT)的发病机制中起重要作用。最近的研究表明,新发现的Th17亚群在自身免疫性疾病的诱导中起重要作用,并且IL-23在Th17细胞上诱导的信号传导对于获得致病性和持续性表型至关重要。本研究的目的是探讨白细胞介素IL-23/IL-17轴在病理过程中的作用。

设计

在疾病活动的不同阶段研究了对照组和HT患者血清中IL-23和IL-17的水平。

对象和方法

我们调查了93例HT患者:33例新诊断的甲状腺功能正常的HT患者(I组),11例新诊断的甲状腺功能减退的HT患者(II组),以及49例接受左甲状腺素治疗的患者(III组)。纳入30名健康受试者作为对照。通过酶联免疫吸附测定法评估患者和对照血清样本中IL-23和IL-17的浓度。

结果

与对照组相比,所有HT患者(p<0.0001)以及患者亚组中的血清IL-23水平均显著升高(p<0.01)。HT患者组血清IL-17浓度有统计学意义的升高(p=0.014);I组和III组与健康对照相比,IL-17水平差异也显著,但II组不显著。

结论

我们的结果突出了IL-23/IL-17轴在HT发生发展及其严重程度中的作用。此外,IL-23分泌上调可能是HT进展和监测的生物标志物。

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