Abstract
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.
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