We identified a novel homozygous missense mutation in IL36RN in two siblings, and showed the molecular basis of the condition to be both distinct from psoriasis and distinct between the two families studied.
Consistently, many psoriasis susceptibility genes encode the TRAF6 signaling players, such as ACT1 (<i>TRAF3IP2</i>), A20 (<i>TNFAIP3</i>), ABIN1 (<i>TNIP1</i>), IL-36Ra (<i>IL36RN</i>), IkappaBzeta (<i>NFKBIZ</i>), and CARD14.
These studies found that IL36RN mutations account for only a fraction of GPP cases presenting with concomitant psoriasis vulgaris (PV; common or typical psoriasis).
Previous studies reported that the interleukin-36 (IL-36) cytokines [IL-36α, IL-36β, IL-36γ and IL-36 receptor antagonists (IL-36RA)] are important players in the pathogenesis of psoriasis (PS).