Overproduction of proinflammatory cytokines plays a significant role in the pathogenesis of Hashimoto's thyroiditis (HT). Recent studies revealed a prominent role of newly discovered Th17 subset in the induction of autoimmune disorders and that the signaling induced by IL-23 on Th17 cells is crucial to obtain a pathogenic and sustained phenotype. The objective of this study was to provide the involvement of interleukin IL-23/IL-17 axis in pathologic processes.Serum levels of IL-23 and IL-17 in controls and HT patients were studied in different stages of disease activity.We investigated 93 patients with HT: 33 patients with newly diagnosed euthyroid HT (Group I), 11 patients with newly diagnosed hypothyroid HT (Group II), and 49 subjects treated with Levothyroxine (Group III). Thirty healthy subjects were included as controls. Concentrations of IL-23 and IL-17 in the serum samples of patients and controls were evaluated by enzyme-linked immunosorbent assay.Serum level of IL-23 was significantly higher in all HT patients (p<0.0001) as well as in subgroups of patients in comparison with controls (p<0.01). Serum concentrations of IL-17 were statistically increased in the group of HT patients (p=0.014); the differences in IL-17 levels between groups I and III in comparison to healthy controls were also significant, but not for group II.Our results highlight the involvement of the IL-23/IL-17 axis in the development of HT and its severity. Moreover, upregulated secretion of IL-23 could be a biomarker for progression and monitoring of HT.