The therapeutic response of pustular psoriasis to biologics supports the pivotal role of the tumor necrosis factor (TNF)-α/interleukin (IL)-23/IL-17/IL-22 axis in the pathogenesis of the disorder.
Although the TNF-?/IL-23/IL-17/IL-22 axis and the functional activation of IL-36R are fundamentally involved in plaque psoriasis and pustular psoriasis, respectively, the 2 pathways are closely related and mutually reinforced, resulting in full-blown clinical manifestations.