Clinical and experimental evidence suggest that interleukin-17A (IL-17A; also 
known as IL-17) is an attractive therapeutic target in rheumatoid arthritis 
(RA). Rheumatoid synovial tissue produces IL-17A, which causes cartilage and 
bone degradation in synovial and bone explants. Overexpression of IL-17A induces 
synovial inflammation and joint destruction in animal RA models. These effects 
are attenuated in IL-17A-deficient animals and by agents that block IL-17A. 
Serum IL-17A levels and, to a greater extent, synovial fluid IL-17A levels are 
elevated in many patients with RA. In some RA cohorts, higher IL-17A levels have 
been associated with a more severe clinical course. Several IL-17A blockers, 
including the anti-IL-17A monoclonal antibodies secukinumab and ixekizumab, and 
the anti-IL-17 receptor subunit A monoclonal antibody brodalumab have been 
evaluated in phase II clinical trials. Of these, secukinumab is the most 
advanced with respect to clinical evaluation in RA, with phase III trials 
ongoing in patients on background methotrexate who had inadequate responses to 
previous tumor necrosis factor blocker therapy.