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

Amgen, Seattle, WA 98119, USA.
The Journal of Immunology (Impact Factor: 5.36). 10/2010; 185(7):4354-62. DOI: 10.4049/jimmunol.1000313
Source: PubMed

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.

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Available from: Muhammad Aslam, Aug 09, 2015
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    • "At the end of the experiment (day 4), mice were killed by cervical dislocation and 1-cm 2 punch biopsies were taken from the treated dorsal skin and weighed in order to measure edema (Amigo et al., 2008). Biopsies were then fixed in formalin for histological study as described previously (Blumberg et al., 2010). "
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