**1. Introduction**

In 1974, the concept of a group that was termed seronegative spondarthritides was first introduced [1] and is now known as Spondyloarthritis (SpA). These heterogeneous rheumatoid-related diseases consist of ankylosing spondylitis (AS), psoriatic spondylitis (PsA), reactive spondylitis (re-SpA), inflammatory bowel disease (IBD)-associated spondylitis, and unclassifiable spondylitis. These diseases share various clinical manifestations including sacroiliac arthritis, spinal arthritis, peripheral arthritis, enthesitis, and extra-articular forms (uveitis, inflammatory bowel disease, and psoriasis [Ps]), and the clinical commonality led to the grouping of these diseases. In addition, after the discovery of IL-23 and IL-17-producing Th17, it was revealed that molecular pathomechanisms were also shared among the different types of SpA.

The pro-inflammatory cytokines IL-23 and IL-17 play an important role in activating the immune response in the host defense against pathogens and maintaining barrier functions of mucosal surfaces. Over the past several years, genetic, experimental, and clinical evidence that SpA was triggered by pathological activation of the IL-23/IL-17 axis has accumulated. Inflammation at the sites of tendon insertion into bone is one of the characteristics of SpA, and it distinguishes SpA from other rheumatoid diseases. Recent studies have suggested the involvement of IL-23 and IL-17 in producing cells with enthesitis. In this review, we focus on the current knowledge of the role of the IL-23/IL-17 pathway in the pathogenesis of SpA and summarize the results of recent clinical trials targeting IL-23 and IL-17 in the treatment of SpA.
