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Role of the tumour necrosis factor‐like weak inducer of apoptosis ( TWEAK )/fibroblast growth factor‐inducible 14 (Fn14) axis in autoimmune thyroid disease
Author(s) -
Peng Shiqiao,
Yu Xiaohui,
Zhao Xuemin,
Wang Xinyi,
Sun Xuren,
Han Cheng,
Shan Zhongyan,
Li Chenyan,
Teng Weiping
Publication year - 2017
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.13404
Subject(s) - pathogenesis , medicine , endocrinology , graves' disease , autoimmune disease , thyroid peroxidase , fibroblast , downregulation and upregulation , peripheral blood mononuclear cell , thyroiditis , receptor , tumor necrosis factor alpha , thyroid , immunology , biology , disease , cell culture , biochemistry , gene , in vitro , genetics
Summary Background TNF ‐like weak inducer of apoptosis ( TWEAK ), its receptor fibroblast growth factor‐inducible 14 (Fn14) and its scavenger receptor CD 163 ( sCD 163) 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 sCD 163 were measured in 38 patients with Graves’ disease ( GD ), 40 patients with Hashimoto's thyroiditis ( HT ) and 40 healthy controls ( HC s). Additionally, the mRNA expression of TWEAK and Fn14 in peripheral blood mononuclear cells ( PBMC s) 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 HC s 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 ( TPOA b) levels. Additionally, high levels of sCD 163 and a high sCD 163/ sTWEAK ratio were positively associated with the TPOA b levels in patients with HT and the thyrotropin receptor antibody ( TRA b) levels in patients with GD . TWEAK mRNA expression and protein expression were upregulated in thyroid glands and PBMC s 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 .