AI Article Synopsis
- Atopic dermatitis (AD) is a chronic skin condition marked by itchy, eczematous lesions due to skin barrier issues and an immune response mediated by T helper (Th)2 cells.
- The cytokine interleukin (IL)-31, mainly produced by Th2 cells, plays a key role in causing itchiness and has been linked to the development of AD-like symptoms in both IL-31 transgenic mice and normal mice treated with IL-31.
- Recent studies have shown that targeting the IL-31 receptor with an anti-IL-31 receptor antibody can significantly reduce itchiness in patients suffering from AD, highlighting the importance of IL-31 and its receptor in the condition.
Article Abstract
Atopic dermatitis (AD) is characterized by chronic, eczematous, severe pruritic skin lesions caused by skin barrier dysfunction and T helper (Th)2 cell-mediated immunity. Interleukin (IL)-31 is a potent pruritogenic cytokine primarily produced by Th2 cells. Both IL-31 transgenic mice and wild-type mice treated with IL-31 exhibit AD-like skin lesions and scratching behaviour. IL-31 receptor α-chain (IL-31RA) is also expressed in peripheral nerves and epidermal keratinocytes, and the roles of IL-31 on pruritus and skin barrier have been investigated. Recently, an anti-IL-31 receptor antibody was shown to significantly improve pruritus in AD patients. This review focuses on IL-31 and IL-31RA in AD.
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| http://dx.doi.org/10.1111/exd.13533 | DOI Listing |
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