Abstract
Our understanding of the pathogenesis of psoriatic arthritis continually evolves, as do the biological treatment options for both psoriasis and psoriatic arthritis. A relatively new pathogenetic pathway involves interleukin 23, playing a role in the very early stages of the pathogenesis of both diseases.
This pathogenetic concept is supported by promising results from blocking this pathway through the selective inhibition of the p19 subunit of interleukin 23, first in the treatment of psoriasis and now in psoriatic arthritis. Recently, the results of some pivotal studies involving risankizumab, a representative of this class of biologic drugs, have been published.
In this article, we provide an overview of these studies and reflect on the position of this biologic within the broader class of interleukin 23 inhibitors.