Research ArticlePsoriasis

An analysis of IL-36 signature genes and individuals with IL1RL2 knockout mutations validates IL-36 as a psoriasis therapeutic target

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Science Translational Medicine  11 Oct 2017:
Vol. 9, Issue 411, eaan2514
DOI: 10.1126/scitranslmed.aan2514

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This article has a correction. Please see:

Nixing IL-36 in psoriasis

Plaque psoriasis is a common T cell–driven autoimmune disease affecting the skin. Targeted biologics impeding the IL-17 inflammatory cytokine family exist but do not provide universal clinical benefit. Mahil et al. convincingly identify IL-36 as an important driver of psoriasis and suggest that blocking IL-36 signaling could bring relief to psoriasis patients. Their results stem from genetic analyses, as well as ex vivo experimentation with patient samples and in vivo treatment of a mouse model. Individuals naturally deficient in IL-36 signaling did not have any overt immunodeficiency, suggesting that interrupting IL-36 would be a safe approach for treating disease.