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J Immunol. 2010 Oct 1;185(7):4354-62. doi: 10.4049/jimmunol.1000313. Epub 2010 Sep 10.

IL-1RL2 and its ligands contribute to the cytokine network in psoriasis.

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  • 1Amgen, Seattle, WA 98119, USA. halb@novonordisk.com

Abstract

Psoriasis is a common immune-mediated disease in European populations; it is characterized by inflammation and altered epidermal differentiation leading to redness and scaling. T cells are thought to be the main driver, but there is also evidence for an epidermal contribution. In this article, we show that treatment of mouse skin overexpressing the IL-1 family member, IL-1F6, with phorbol ester leads to an inflammatory condition with macroscopic and histological similarities to human psoriasis. Inflammatory cytokines thought to be important in psoriasis, such as TNF-α, IL-17A, and IL-23, are upregulated in the mouse skin. These cytokines are induced by and can induce IL-1F6 and related IL-1 family cytokines. Inhibition of TNF or IL-23 inhibits the increased epidermal thickness, inflammation, and cytokine production. Blockade of IL-1F6 receptor also resolves the inflammatory changes in human psoriatic lesional skin transplanted onto immunodeficient mice. These data suggest a role for IL-1F family members in psoriasis.

PMID:
20833839
[PubMed - indexed for MEDLINE]
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