Genetic studies and correlative expression data in diseased tissues have pointed 
to the role of interleukin (IL)-17 and Th17 cells in the pathogenesis of 
autoimmune disorders such as psoriasis, inflammatory bowel disease and 
seronegative spondyloarthropathies. Th17 cells are known to produce the 
proinflammatory cytokine IL-17A as well as other effector cytokines, including 
IL-17F and IL-22. Recent research has demonstrated that IL-17A is also expressed 
by multiple lineages of the innate immune system, including mast cells, 
neutrophils, dendritic cells, γδ-T cells, macrophages and natural killer cells. 
It can thus be expected that the inhibition of IL-17A as a therapeutic target in 
autoimmune disease would exert different physiological effects than the 
suppression of Th17 cell activity. Early clinical data are now available on 
secukinumab (AIN457), a recombinant, highly selective, fully human monoclonal 
anti-IL-17A antibody of the IgG1/κ isotype, enabling a preliminary assessment of 
the effects of IL-17A inhibition in multiple autoimmune diseases. Rapid and 
sustained symptom reductions in psoriasis, rheumatoid arthritis, psoriatic 
arthritis and ankylosing spondylitis have been observed in secukinumab-treated 
patients, with no overt safety signals. In conjunction with studies using the 
humanised anti-IL-17A monoclonal antibody (mAb) ixekizumab (LY2439821) and the 
fully human anti-IL-17RA mAb brodalumab (AMG 827), the findings on secukinumab 
provide evidence for the role of IL-17A in the pathophysiology of autoimmune 
disease and suggest the potential value of targeting this cytokine.