Nevertheless, a number of knowledge gaps exist regarding the role of IL-17A in the pathophysiology of spondyloarthritis in man, including its cellular origin, its precise role in discrete disease processes such enthesitis, bone erosion, and bone formation, and the reasons for the discrepant responses to IL-17A inhibition observed in certain other spondyloarthritis manifestations.
Cytokines from the IL-17 family have been shown to be involved in the pathogenesis of several diseases such as spondyloarthritis, psoriatic arthritis, or psoriasis.
Murine models of interleukin (IL)-23-driven spondyloarthritis (SpA) have demonstrated entheseal accumulation of γδT-cells which were responsible for the majority of local IL-17A production.
Despite a ballooning therapeutic tool box, treatment responses to newer biologic agents and oral small molecules in psoriatic arthritis (PsA) and spondyloarthritis (SpA) are of similar magnitude to those observed with anti-Tumor Necrosis Factor (TNF) medications (1, 2).The PsA and SpA therapeutic outcomes stand in marked contrast to those reported in psoriasis where blockade of molecules in the IL-23/IL-17 pathway often provide prolonged, deep responses and in some cases even remission (3).