Purpose of Review: Atopic dermatitis (AD) is a chronic eczematous skin disease associated with intense pruritus and skin barrier dysfunction. Interleukin-31 (IL-31), which is preferentially produced by T helper 2 (Th2) cells, has attracted attention as a pruritogen in patients with AD. To understand the mechanism of action, production, and roles of IL-31, we reviewed recent advances of the knowledge of IL-31, its receptor as well as results of recent clinical trials targeting IL-31/IL-31R signaling for pruritus in patients with AD. Recent Findings: Activation of many cytokine pathways has been reported in AD, suggesting potential therapeutic targets with novel biologics. Most notably, the lesional skin of AD exhibits Th2-deviated immune reactions. Recently reported striking efficacy of dupilumab, a monoclonal antibody targeting the IL-4 receptor α subunit reconfirms the importance of Th2-deviated immune reactions in the pathogenesis of AD. A systemic and local administration of IL-31 induces scratching behavior in mice, dogs, and monkeys. In addition, serum levels of IL-31 have been correlated with severity of AD. Finally, an anti-interleukin (IL)-31 receptor α antibody (nemolizumab) has been shown to significantly alleviate pruritus in AD patients. Summary: The interaction between IL-31 and IL-31R has a role not only in the induction of intense pruritus, but also in the regulation of inflammation and barrier function in AD. In clinical trials, nemolizumab significantly improved pruritus in patients with moderate-to-severe AD. Targeting the IL-31/IL-31R interaction might be a promising therapeutic target to improve the burdensome pruritus experienced by patients with AD.
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