Introduction: We aimed to investigate the role of sTWEAK in the pathogenesis of Hashimoto’s thyroiditis, which is a chronic inflammatory autoimmune disease.

Material and methods: A total of 80 patients were included in the study, 60 of whom were newly diagnosed with Hashimoto’s thyroiditis (20 patients in each of the euthyroid, subclinical hypothyroid, and overt hypothyroid subgroups), and 20 of whom were healthy volunteers. Thyroid function tests and autoantibodies were measured using the electro-chemiluminescence immunoassay method, and sTWEAK, IL-17A, IL-12, and TGF-beta1 were measured using enzyme-linked immunosorbent assay method.

Results: The Hashimoto’s Thyroiditis group had lower levels of sTWEAK and TGF-beta1, but had higher levels of IL-12 and IL-17A as compared to the control group. Of these, only the difference between IL-17A levels reached statistical significance (2.1 pg/mL vs. 1.8 pg/mL, respectively; p < 0.001). While the levels of sTWEAK were similar in the control, euthyroid, and subclinical groups, the overt hypothyroidism group had lower level of sTWEAK than that of subclinical hypothyroidism (687.6 ± 153.3 pg/mL vs. 888.2 ± 374.4 pg/mL, respectively; p = 0.03). A negative correlation was determined between sTWEAK level and anti-TPO (r = –0.533, p = 0.028) and IL-17A (r = –0.600, p = 0.005) levels in the overt hypothyroidism group.

Conclusions: The reduced levels of sTWEAK with progression of Hashimoto’s Thyroiditis and the significant correlation between the sTWEAK levels and anti-TPO found in this study suggest that sTWEAK plays an active role in chronic inflammation in the pathogenesis of Hashimoto’s Thyroiditis and in the progression of autoimmunity. (Endokrynol Pol 2016; 67 (6): 562–566)