IL-36 in psoriasis

Psoriasis is a common but severe skin disease with significant health consequences, both physical and psychological. Evidence has emerged during the past several years pointing to a key role for IL-36 in psoriasis. Overexpression of IL-36 in mouse skin leads to a disease quite similar to human plaque psoriasis, and inhibition of IL-36 in human psoriatic skin ameliorates the inflammation. Loss of the natural antagonist of IL-36, IL-36Ra, results in a different, more severe skin disease known as pustular psoriasis. These effects are likely a consequence of the actions of IL-36 both on cells of the immune system as well as on components of skin including fibroblasts and keratinocytes.

► A new mouse model provides extensive support for a role of IL-36 in human plaque psoriasis.
► Further evidence comes from in vitro studies in multiple laboratories.
► Separately, reduction-in-function mutations in IL-36Ra have been implicated in generalized pustular psoriasis.
► Recent studies suggest activity of IL-36 in multiple additional organ systems, including lung, kidney and immune function.