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

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 HT patients and inversely correlated with anti-thyroid peroxidase antibody (TPOAb) levels. Additionally, high levels of sCD163 and a high sCD163/sTWEAK ratio were positively associated with the TPOAb levels in HT patients and the thyrotropin receptor antibody (TRAb) levels in GD patients. TWEAK mRNA and protein expression were up-regulated in thyroid glands and PBMCs from HT patients. Conclusion Expression of the TWEAK-Fn14 axis was up-regulated in patients with AITD and might play a role in the pathogenesis of AITD. This article is protected by copyright. All rights reserved.