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A role for IL-25 and IL-33-driven type-2 innate lymphoid cells in atopic dermatitis.

机译:IL-25和IL-33驱动的2型先天性淋巴样细胞在特应性皮炎中的作用。

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摘要

Type 2 innate lymphoid cells (ILC2s, nuocytes, NHC) require RORA and GATA3 for their development. We show that human ILC2s express skin homing receptors and infiltrate the skin after allergen challenge, where they produce the type 2 cytokines IL-5 and IL-13. Skin-derived ILC2s express the IL-33 receptor ST2, which is up-regulated during activation, and are enriched in lesional skin biopsies from atopic patients. Signaling via IL-33 induces type 2 cytokine and amphiregulin expression, and increases ILC2 migration. Furthermore, we demonstrate that E-cadherin ligation on human ILC2 dramatically inhibits IL-5 and IL-13 production. Interestingly, down-regulation of E-cadherin is characteristic of filaggrin insufficiency, a cardinal feature of atopic dermatitis (AD). ILC2 may contribute to increases in type 2 cytokine production in the absence of the suppressive E-cadherin ligation through this novel mechanism of barrier sensing. Using Rag1-/-and RORα-deficient mice, we confirm that ILC2s are present in mouse skin and promote AD-like inflammation. IL-25 and IL-33 are the predominant ILC2-inducing cytokines in this model. The presence of ILC2s in skin, and their production of type 2 cytokines in response to IL-33, identifies a role for ILC2s in the pathogenesis of cutaneous atopic disease.
机译:2型先天淋巴样细胞(ILC2,核细胞,NHC)需要RORA和GATA3才能发育。我们显示,人类ILC2s表达皮肤归巢受体并在变应原攻击后浸润皮肤,在那里它们产生2型细胞因子IL-5和IL-13。皮肤来源的ILC2表达IL-33受体ST2,该信号在激活过程中被上调,并且富含特应性患者的病灶皮肤活检。通过IL-33发出的信号会诱导2型细胞因子和双调蛋白表达,并增加ILC2迁移。此外,我们证明E-钙粘着蛋白对人ILC2的连接可显着抑制IL-5和IL-13的产生。有趣的是,E-钙黏着蛋白的下调是聚连蛋白功能不全的特征,这是特应性皮炎(AD)的主要特征。在这种抑制性E-cadherin抑制性连接不存在的情况下,ILC2可能有助于增加2型细胞因子的产生。使用Rag1-/-和RORα缺陷型小鼠,我们证实ILC2s存在于小鼠皮肤中并促进AD样炎症。 IL-25和IL-33是此模型中主要的ILC2诱导细胞因子。皮肤中ILC2的存在及其对IL-33的2型细胞因子的产生,确定了ILC2在皮肤异位性疾病发病机理中的作用。

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