New possibilities of pharmacotherapy for immunoinflammatory rheumatic diseases: a focus on inhibitors of interleukin-17

In recent years, more attention has been focused on Тh17 cells that synthesize interleukin-17 (IL-17) in contrast to Тh1 and Тh2 cells, the marker cytokines of which are interferon-ү (IFN-ү) and IL-4, respectively. It is precisely these pathological activation and expansion of ТҺ17 cells that are supposed to play a key role in the development of a wide spectrum of human immunoinflammatory diseases (IIDs), including rheumatoid arthritis (RA), psoriasis, ankylosing spondylitis (AS), psoriatic arthritis (PsA), inflammatory bowel disease, and systemic lupus erythematosus, which were previously considered as Тh1-dependent diseases associated primarily with the hyperproduction of IL-2 and IFN-ү. This has served as a powerful stimulus to design new biological agents, the mechanism of action of which is based on blocking the pathological effects of IL-17, others associated with the activation of Тh17 cells of cytokines, or small molecules interfering with transcription factors that regulate the synthesis of these cytokines. This review discusses current studies of the mechanisms regulating the formation and functional activity of IL-17 family cytokines, as well as evidence of the importance of these cytokines in the pathogenesis of IIDs. Special attention is paid to the clinical efficacy and safety of anti-IL-17A monoclonal antibody secukinumab used to treat psoriasis, PsA, AS, and RA.