Vidal, SilviaPuig, LluísCarrascosa-Carrillo, José-ManuelGonzález-Cantero, ÁlvaroRuiz-Carrascosa, José-CarlosVelasco-Pastor, Antonio-Manuel2023-02-092023-02-092021-06-23http://hdl.handle.net/10668/18086The paradigm of psoriasis as a Th17-driven disease has evolved in the last years towards a much deeper knowledge of the complex pathways, mechanisms, cells, and messengers involved, highlighting the crucial role played by the IL-17 family of cytokines. All IL-17 isoforms signal through IL-17R. Five subunits of IL-17R have been described to date, which couple to form a homo- or hetero-receptor complex. Characteristically, IL-17RA is a common subunit in all hetero-receptors. IL-17RA has unique structural-containing a SEFIR/TILL domain-and functional-requiring ACT-1 for signaling-properties, enabling Th17 cells to act as a bridge between innate and adaptive immune cells. In psoriasis, IL-17RA plays a key role in pathogenesis based on: (a) IL-17A, IL-17F, and other IL-17 isoforms are involved in disease development; and (b) IL-17RA is essential for signaling of all IL-17 cytokines but IL-17D, whose receptor has not been identified to date. This article reviews current evidence on the biology and role of the IL-17 family of cytokines and receptors, with focus on IL-17RA, in psoriasis and some related comorbidities, and puts them in context with current and upcoming treatments.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/IL-17IL-17RTh17bimekizumabbrodalumabixekizumabmonoclonal antibodiespsoriasissecukinumabAntibodies, Monoclonal, HumanizedHumansInterleukin-17Protein IsoformsPsoriasisReceptors, Interleukin-17research article34201664open access10.3390/ijms221367401422-0067PMC8268646https://www.mdpi.com/1422-0067/22/13/6740/pdf?version=1646040180https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8268646/pdf