Psoriasis is a chronic inflammatory skin disease affecting about 1-3% of the 
general population. Moderate-to-severe psoriasis is commonly associated with 
various comorbidities, including psoriatic arthritis (PsA) and cardio-metabolic 
disorders such as obesity, hypertension, diabetes, and metabolic syndrome. There 
is increasing recognition that systemic inflammation accompanies severe skin 
disease. Abnormal innate and adaptive immune responses in the skin are involved 
in pathogenesis. The cytokine interleukin (IL)-17A is produced by T helper 17 
(Th17) cells, neutrophils, mast cells, and T cytotoxic 17 cells. IL-17 plays a 
key role in host defense against extracellular bacteria and fungi. IL-17A acts 
on keratinocytes to increase expression of chemokines involved in recruiting 
myeloid dendritic cells, Th17 cells, and neutrophils to the lesion site. IL-17A 
also induces the production of antimicrobial peptides and pro-inflammatory 
cytokines that, in turn, may amplify and sustain immune responses in the skin. 
Blocking IL-17A improved psoriasis-like pathology in experimental models, and 
reduction in IL-17 signaling is part of the mechanism of action of tumor 
necrosis factor-α blockers. Three agents neutralizing IL-17 (i.e., secukinumab 
and ixekizumab) or antagonizing its receptor (i.e., brodalumab) are currently 
being tested for efficacy and safety in the treatment of plaque psoriasis and 
PsA. Secukinumab is a fully human IgG1 monoclonal antibody that selectively 
binds and neutralizes IL-17A whose efficacy in the therapy of chronic plaque 
psoriasis has been demonstrated in different phase II clinical trial. No new 
safety signals have emerged so far.