Abstract
Interleukin-17 (IL-17) is an essential proinflammatory cytokine, which is mainly secreted by the CD4+ helper T cells (Th17 cells) and subsets of innate lymphoid cells. IL-17A is associated with the pathogenesis of inflammatory diseases, including psoriasis, atopic dermatitis, hidradenitis suppurativa, alopecia areata, pityriasis rubra pilaris, pemphigus, and systemic sclerosis. Interleukin-23 (IL-23) plays a pivotal role in stimulating the production of IL-17 by activating the Th17 cells. The IL-23/IL-17 axis is an important pathway for targeted therapy for inflammatory diseases. Emerging evidence from clinical trials has shown that monoclonal antibodies against IL-23, IL-17, and tumor necrosis factor are effective in the treatment of patients with psoriasis, atopic dermatitis, hidradenitis suppurativa, pityriasis rubra pilaris, pemphigus, and systemic sclerosis. Here, we summarize the latest knowledge about the biology, signaling, and pathophysiological functions of the IL-23/IL-17 axis in inflammatory skin diseases. The currently available biologics targeting the axis is also discussed.
Highlights
Interleukin-17A (IL-17A) is cloned from a T cell hybridoma activated in rodents [1] and is related to several immune-mediated disorders, such as autoimmune [2], oncogenic [3], and infectious [4] diseases
According to the data from phase III studies (SPIRIT-P1 and SPIRIT-P2), ixekizumab is associated with improvements in disease prognosis and physical function in patients with active psoriatic arthritis (PsA), in those who are refractory to therapies or have an inadequate response to the anti-tumor necrosis factor (TNF) therapies (Supplementary Table) [85, 86]
An open-label study involving 39 patients with moderate-to-severe psoriasis revealed that brodalumab treatment may be effective for the patients who did not respond to secukinumab, ixekizumab, or ustekinumab [91, 92]
Summary
Interleukin-17A (IL-17A) is cloned from a T cell hybridoma activated in rodents [1] and is related to several immune-mediated disorders, such as autoimmune [2], oncogenic [3], and infectious [4] diseases. The data from the phase III randomized trials (ERASURE and FIXTURE) showed that secukinumab at doses of 300 or 150 mg is effective and safe for the treatment of moderate-to-severe psoriasis up to week 52 (Supplementary Table) [77]. In the FUTURE 2 study, patients with PsA receiving secukinumab therapy achieved excellent and sustained improvement in the PASI90 and American College of Rheumatology 50 (ACR50) response at week 24 (Supplementary Table) [79].
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