This article presents analysis of current data highlighted the problem of pathogenic mechanism of the most common spondyloarthritides (SpA) and focused on the pivotal role of interleukin‑17 in immune inflammation realization. Contribution of IL‑17 in mechanism of SpA particularly in different organ damage, in perpetuation of chronic inflammation and in structural progression is discussed. The clinical and experimental evidence of close relationship between IL‑17A levels, on one hand, and disease activity, high tempo of joint and bone affection as well as SpA extra-articular manifestations, on the other, are presented. Contribution of cell-mediated immune response including activated IL‑17A-producing cells to the pathogenesis of different SpA phenotypes is shown. Great attention is paid to the clinical effects of IL‑17A inhibition in Sp A. The results of clinical trials of novel IL‑17A inhibitor netakimab in the treatment of ankylosing spondylitis are presented. These data have demonstrated high efficacy and safety of tried preparation used in the regimen 120 mg per 2 weeks. On the basis of performed analysis the key role of IL‑17 in SpA pathogenesis is confirmed and expediency of SpA target therapy with novel IL‑17A inhibitor netakimab is justified.