Abstract
Spondyloarthritis (SpA) is a subset of seronegative rheumatic-related autoimmune diseases that consist of ankylosing spondylitis (AS), psoriatic spondylitis (PsA), reactive spondylitis (re-SpA), inflammatory bowel disease (IBD)-associated spondylitis, and unclassifiable spondylitis. These subsets share clinical phenotypes such as joint inflammation and extra-articular manifestations (uveitis, IBD, and psoriasis [Ps]). Inflammation at the enthesis, where ligaments and tendons attach to bones, characterizes and distinguishes SpA from other types of arthritis. Over the past several years, genetic, experimental, and clinical studies have accumulated evidence showing that the IL-23/IL-17 axis plays a critical role in the pathogenesis of SpA. These discoveries include genetic association and the identification of IL-23- and IL-17-producing cells in the tissue of mouse models and human patients. In this review, we summarize the current knowledge of the pathomechanism by focusing on the IL-23/IL-17 pathway and examine the recent clinical studies of biological agents targeting IL-23 and IL-17 in the treatment of SpA.
Highlights
In 1974, the concept of a group that was termed seronegative spondarthritides was first introduced [1] and is known as Spondyloarthritis (SpA)
The results suggest that the interactions between HLA-B27 and the microbiome are relevant to the pathogenesis of SpA
Hayashi et al demonstrated the correlation between the expression of CD69 on Mucosa-Associated Invariant T (MAIT) cells with the Ankylosing Spondylitis Disease Activity Score (ASDAS) in patients with ankylosing spondylitis (AS). These results suggest that the upregulation of IL-17 by MAIT cells contributes to the pathogenesis of SpA
Summary
In 1974, the concept of a group that was termed seronegative spondarthritides was first introduced [1] and is 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. IInn tthhee 11997700ss,, sseevveerraall ddiiaaggnnoossttiicc ccrriitteerriiaa wweerree pprrooppoosseedd ttoo ddeefifinnee ppaattiieennttss wwiitthh aa ssppeecciifificc ssuubbttyyppee ooff SSppAA,, ssuucchh aass tthhee mmooddiififieedd NNeeww YYoorrkkccrriitteerriiaaffoorrAASS[[22,3,3]]. HLA-B27, one of the proteins belonging to MHC class I, was first reported to associate with AS in 1973 and is considered the essential genetic factor in the pathogenesis of SpA [9]. Variants of STAT3 and Tyk, which are downstream targets of IL-23, have been reported to be associated with AS and PsA [14,19,20]
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