Insight into the role of two proteins in psoriasis means a rethink in treatments is necessary
A skin condition characterised by scaly red patches, psoriasis is an autoimmune disorder linked to dysfunctional immune signalling, causing inflammation and accelerating cell division in the outermost layer of skin, the epidermis. Treatments targeting a shared feature of signalling proteins interleukin-12 (IL-12) and interleukin-23 (IL-23) can alleviate symptoms, but later drugs affecting only IL-23 proved even more effective, prompting questions about the role of IL-12. By selectively deleting the receptor for IL-12 in epidermal skin cells, keratinocytes, in mice, researchers showed that IL-12 actually protects against psoriasis. In the skin samples above, dividing keratinocytes in the epidermis (left of the white line), are highlighted in red; cells possessing the IL-12 receptor (left panel) are dividing less than those lacking it (right), suggesting that IL-12 acts to reduce cell proliferation. Future therapies should therefore concentrate on IL-23, a result with potential implications for other conditions treated by blocking both proteins.
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