"Psoriasis" is a chronic immune-mediated inflammatory disorder with epidermal 
hyperplasia. There is some evidence that the cytokine interleukin-17A (often 
known as IL-17), which is mainly produced by Th17 cells, has a role in the 
pathogenesis of psoriasis. "IL-17" is a pro-inflammatory cytokine mainly 
important in the host's defense against extracellular bacteria and fungi. The 
three new therapies with biologic drugs - brodalumab, secukinumab, and 
ixekizumab - all target the IL-17 signaling pathway. Secukinumab and ixekizumab 
neutralize IL-17A, while brodalumab blocks its receptor. Results from clinical 
trials have shown marked improvements in disease severity in patients with 
moderate-to-severe plaque psoriasis, using any of these three drugs. The 
biologic agents were generally well tolerated, but the duration of the trials 
was relatively short. In this review, we focus on the role of the IL-17 cytokine 
family in the pathogenesis of psoriasis; the efficacy, safety, and tolerability 
of brodalumab, secukinumab, and ixekizumab in clinical trials; and possible 
differences between targeting of the IL-17A receptor and targeting of the IL-17A 
ligand.