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IL-13Rα2 在特应性皮炎皮肤炎症中的意义。

Implications of IL-13Rα2 in atopic skin inflammation.

机构信息

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Division of Skin Surface Sensing, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, Fukuoka, Japan.

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

出版信息

Allergol Int. 2020 Jul;69(3):412-416. doi: 10.1016/j.alit.2020.01.005. Epub 2020 Feb 6.

Abstract

Atopic dermatitis (AD) is a common eczematous skin disorder characterized by skin inflammation, barrier disruption, chronic pruritus and marked scratching. Th2 cytokines, especially IL-13, play a pathogenic role in AD. IL-13 signals via a heterodimeric receptor composed of IL-4Rα and IL-13 Rα1. A second receptor, IL-13 Rα2, binds to IL-13 with high affinity, but it works as a decoy receptor. IL-13 Rα2 is overexpressed in the lesional skin of AD. Notably, mechanical scratching, as well as IL-13 itself, also upregulates IL-13 Rα2 expression. The scratch-induced IL-13 Rα2 upregulation may attenuate the IL-13-mediated epidermal barrier dysfunction and dermal fibrosis. Recent studies stress an importance of another IL-13 Rα2 ligand, chitinase 3-like 1 or YKL-40 in Th2 differentiation. However, the implications of increased IL-13 Rα2 levels remain elusive in AD. In this review, we summarize the recent topics on IL-13 Rα2 in atopic skin inflammation.

摘要

特应性皮炎(AD)是一种常见的湿疹性皮肤疾病,其特征为皮肤炎症、屏障破坏、慢性瘙痒和明显搔抓。Th2 细胞因子,尤其是白细胞介素-13(IL-13),在 AD 中发挥致病作用。IL-13 通过由 IL-4Rα 和 IL-13Rα1 组成的异二聚体受体信号转导。第二个受体,IL-13Rα2,与 IL-13 具有高亲和力结合,但它作为诱饵受体发挥作用。IL-13Rα2 在 AD 的皮损皮肤中过度表达。值得注意的是,机械搔抓以及 IL-13 本身也会上调 IL-13Rα2 的表达。搔抓诱导的 IL-13Rα2 上调可能会减弱 IL-13 介导的表皮屏障功能障碍和真皮纤维化。最近的研究强调了另一种 IL-13Rα2 配体,几丁质酶 3 样 1 或 YKL-40 在 Th2 分化中的重要性。然而,AD 中增加的 IL-13Rα2 水平的影响仍不清楚。在这篇综述中,我们总结了最近关于特应性皮炎中 IL-13Rα2 的研究进展。

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