A review of JAK-STAT signalling in the pathogenesis of spondyloarthritis and the role of JAK inhibition
McInnes IB, Szekanecz Z, McGonagle D, Maksymowych WP, Pfeil A, Lippe R, Song IH, Lertratanakul A, Sornasse T, Biljan A, Deodhar A. - Rheumatology (Oxford). 2021. Epub ahead of print. doi: 10.1093/rheumatology/keab740.
JAK inhibitors are likely to become an important part of the overall treatment paradigm for spondyloarthritis (SpA).
Although not fully understood, the pathogenesis of SpA is complex and thought to involve both environmental and genetic factors that together elicit a chronic inflammatory response involving the innate and adaptive immune systems. Several different cytokines, TNF, IL-17A, IL-12/23 and IL-23, which are directly/indirectly affected by JAK molecules, are involved in the pathogenesis of SpA. As such, JAK inhibitors are an emerging class of oral small molecule treatments that have demonstrated efficacy in SpA, with several molecules now approved or in late-phase clinical development.
To this end, McInnes, et al. provide a timely review of the role of JAK-STAT signalling in the pathogenesis of SpA and the evidence from clinical trials of JAK inhibitors in patients with SpA.