Atopic dermatitis (AD) is a common inflammatory skin condition that has traditionally been considered a paradigmatic type 2 immunity (T2)‐driven disease. Interleukin (IL)‐4 and IL‐13 are both pivotal cytokines involved in the generation of allergic diseases. Currently, besides dupilumab, which blocks the binding of both cytokines to their receptors, a number of new pharmacologic entities have been designed to target both T2 cytokines and/or their receptors and/or receptor‐associated signal transduction machinery such as Janus kinases. Recently, IL‐13 has been suggested to be the key T2 cytokine driving inflammation in the periphery, while IL‐4 may merely have a central effect. There is increasing evidence that this concept holds true for the inflammatory reaction underlying AD, where IL‐13 is overexpressed locally and has a significant impact on skin biology, including the recruitment of inflammatory cells, the alteration of the skin microbiome, and the decrease in the epidermal barrier function. This review provides an update on the role of IL‐13 in AD and discusses the different strategies aimed at interfering with its biologic activity as well as their potential in a precision medicine approach in the management of AD.

中文翻译：

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Interleukin-13：靶向特应性皮炎中被低估的细胞因子

特应性皮炎 (AD) 是一种常见的炎症性皮肤病，传统上被认为是典型的 2 型免疫 (T2) 驱动的疾病。白细胞介素 (IL)-4 和 IL-13 都是参与过敏性疾病发生的关键细胞因子。目前，除了阻断两种细胞因子与其受体结合的 dupilumab 之外，还设计了许多新的药理学实体来靶向 T2 细胞因子和/或其受体和/或受体相关的信号转导机制，如 Janus 激酶。最近，IL-13 被认为是驱动外周炎症的关键 T2 细胞因子，而 IL-4 可能仅具有中枢作用。越来越多的证据表明，这一概念适用于 AD 潜在的炎症反应，其中 IL-13 在局部过度表达并对皮肤生物学有显着影响，包括炎症细胞的募集、皮肤微生物组的改变和表皮屏障功能的降低。本综述更新了 IL-13 在 AD 中的作用，并讨论了旨在干扰其生物学活性的不同策略，以及它们在 AD 管理中的精准医学方法中的潜力。