Role of the tumour necrosis factor‐like weak inducer of apoptosis ( TWEAK )/fibroblast growth factor‐inducible 14 (Fn14) axis in autoimmune thyroid disease

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 .