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Nakashima, Chisa; Otsuka, Atsushi; Kabashima, Kenji
Experimental dermatology, April 2018, 2018-04-00, 20180401, Volume: 27, Issue: 4Journal Article
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.
