PURPOSE OF REVIEW: In recent years, there has been an increasing understanding 
of the importance of the TH17 lineage of T cells and related cytokines, 
including interleukin (IL)17 and IL23, not only in the biology of innate host 
defense but also in the pathogenesis of inflammatory/autoimmune diseases. These 
diseases include psoriasis, psoriatic arthritis, the broader category of 
spondyloarthritides including ankylosing spondylitis and rheumatoid arthritis. 
It is postulated that in genetically predisposed individuals, external or 
internal stimuli such as microbial antigens, alterations in the intestinal 
microbiome, biomechanical stress and/or immunologic dysregulation may lead to an 
increased expression of cytokines such as IL23, which in turn stimulate the 
differentiation and activation of TH17 and other immune cells, which are a part 
of the innate immune system that trigger adaptive immune processes and chronic 
inflammatory diseases. Herein, we explore the effect of targeting this pathway 
therapeutically.
RECENT FINDINGS: New drugs that are designed to inhibit steps in this pathway, 
the IL12/IL23 inhibitor, ustekinumab, the IL17A inhibitors secukinumab and 
ixekizumab, the IL17A receptor inhibitor, brodalumab, and the IL23 inhibitors 
guselkumab and tildrakizumab, have demonstrated significant effectiveness in 
treating these diseases, particularly psoriasis, psoriatic arthritis and 
ankylosing spondylitis.
SUMMARY: This article reviews the relevant biology, efficacy and safety of new 
medications targeting the TH17 pathway, including inhibition of IL17 and IL23, 
particularly in psoriasis and psoriatic arthritis. Especially for patients who 
have not gained benefit from, lost effectiveness to or could not use antitumour 
necrosis factor (TNF) medications for safety or tolerability reasons, having 
effective medicines with an alternative mechanism of action will improve our 
ability to diminish disease activity impact on patient lives.