PURPOSE OF REVIEW: Various novel therapies for spondyloarthritis (SpA) are 
currently under development. In this review, we discuss the scientific rational 
to target the interleukin (IL)-23/IL-17 axis in SpA and give an overview of the 
proof-of-concept trials with drugs directed towards this axis.
RECENT FINDINGS: Cumulative evidence from genetics (e.g. the strong genetic 
association with the IL-23 receptor gene), in-vitro models (e.g. the increased 
IL-23 production upon HLA-B27 misfolding), human expression studies (e.g. the 
expansion of IL-17 producing innate cells in SpA) and animal models (e.g. the 
increased IL-17 production in HLA-B27 transgenic rats) strongly supports the 
involvement of the IL-23/IL-17 axis in the pathogenesis of SpA. Ustekinumab (a 
monoclonal antibody directed against the common p40 subunit of IL-23 and IL-12), 
secukinumab, ixekizumab (both monoclonal antibodies directed against IL-17A), 
and brodalumab a monoclonal antibody against the IL-17RA receptor) have been 
recently used in proof-of-concept and randomized trials in the ankylosing 
spondylitis and/or psoriatic arthritis subforms of SpA, with overall very 
promising clinical efficacy.
SUMMARY: The first results for novel drugs blocking key cytokines in the 
IL-23/IL-17 axis are promising in SpA and more novel compounds are upcoming. 
This will teach us more on the role of the IL-23/IL-17 axis in the 
pathophysiology of SpA.