肿瘤坏死因子样凋亡弱诱导因子（TWEAK）/成纤维细胞生长因子诱导 14（Fn14）轴在自身免疫性甲状腺疾病中的作用。
Role of the tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible 14 (Fn14) axis in autoimmune thyroid disease.
机构信息
Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang, Liaoning, China.
Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang, Liaoning, China.
出版信息
Clin Endocrinol (Oxf). 2017 Dec;87(6):783-790. doi: 10.1111/cen.13404. Epub 2017 Jul 28.
BACKGROUND
TNF-like weak inducer of apoptosis (TWEAK), its receptor fibroblast growth factor-inducible 14 (Fn14) and its scavenger receptor CD163 (sCD163) have known associations with many autoimmune diseases. However, the role of the TWEAK axis in autoimmune thyroid disease (AITD) remains unclear. Therefore, the aim of this study was to investigate the role of the TWEAK-Fn14 axis in the pathogenesis of AITD.
METHODS
Serum levels of soluble TWEAK (sTWEAK) and sCD163 were measured in 38 patients with Graves' disease (GD), 40 patients with Hashimoto's thyroiditis (HT) and 40 healthy controls (HCs). Additionally, the mRNA expression of TWEAK and Fn14 in peripheral blood mononuclear cells (PBMCs) was explored, and the protein expression of TWEAK and Fn14 in thyroid glands surgically removed from 10 patients with GD, 10 patients with HT and 10 HCs was studied by immunohistochemical staining.
RESULTS
The results showed that the serum levels of sTWEAK were significantly reduced in patients with HT and inversely correlated with antithyroid peroxidase antibody (TPOAb) levels. Additionally, high levels of sCD163 and a high sCD163/sTWEAK ratio were positively associated with the TPOAb levels in patients with HT and the thyrotropin receptor antibody (TRAb) levels in patients with GD. TWEAK mRNA expression and protein expression were upregulated in thyroid glands and PBMCs from patients with HT.
CONCLUSION
Expression of the TWEAK-Fn14 axis was upregulated in patients with AITD and might play a role in the pathogenesis of AITD.
背景
TNF 样弱凋亡诱导因子（TWEAK）、其受体成纤维细胞生长因子诱导 14（Fn14）及其清道夫受体 CD163（sCD163）与许多自身免疫性疾病有关。然而，TWEAK 轴在自身免疫性甲状腺疾病（AITD）中的作用尚不清楚。因此，本研究旨在探讨 TWEAK-Fn14 轴在 AITD 发病机制中的作用。
方法
检测 38 例格雷夫斯病（GD）患者、40 例桥本甲状腺炎（HT）患者和 40 例健康对照者（HCs）的血清可溶性 TWEAK（sTWEAK）和 sCD163 水平。同时，探讨外周血单个核细胞（PBMCs）中 TWEAK 和 Fn14 的 mRNA 表达，并通过免疫组织化学染色研究 10 例 GD、10 例 HT 和 10 例 HCs 手术切除甲状腺组织中 TWEAK 和 Fn14 的蛋白表达。
结果
结果显示，HT 患者血清 sTWEAK 水平显著降低，与抗甲状腺过氧化物酶抗体（TPOAb）水平呈负相关。此外，HT 患者 sCD163 水平升高和 sCD163/sTWEAK 比值升高与 TPOAb 水平以及 GD 患者促甲状腺素受体抗体（TRAb）水平呈正相关。HT 患者甲状腺组织和 PBMCs 中 TWEAK mRNA 表达和蛋白表达上调。
结论
AITD 患者 TWEAK-Fn14 轴表达上调，可能在 AITD 的发病机制中发挥作用。
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