IL-33对特应性皮炎患者ST2-ILC2s轴及皮肤屏障影响的研究进展

Advances in the influence of IL-33 on ST2-ILC2s axis and skin barrier in atopic dermatitis

特应性皮炎(AD)是目前最常见、反复发作、对生活质量影响较大的免疫性皮肤病之一。IL-33是IL-1家族成员之一,上皮细胞会因机械创伤、细菌和外源性蛋白酶等触发因素释放IL-33,IL-33通过长型血清刺激因子-2(ST2)和多种细胞上的IL-1受体附件结合,并激活第2组固有淋巴细胞(ILC2s)、Th2细胞、肥大细胞等,产生系列细胞因子,促使嗜酸性粒细胞浸润,导致AD表症发生和加重。另外,IL-33可能作用于AD表皮屏障功能受损-反复瘙痒循环。为了进一步探究AD的分子机制,寻求新的药物使用策略,提高AD的治疗效能,本文从多个方面阐述IL-33在AD致病、发展过程中的重要作用。

Currently,atopic dermatitis(AD)is one of the most common and recurrent immune dermatoses that greatly impact the quality of life.IL-33,a member of the IL-1 family,is released from epithelial cells upon mechanical trauma,bacterial infections and exposure to exogenous proteases.IL-33 binds to IL-1 receptor accessory protein on a variety of cells through ST2,activating group 2 natural lymphocytes,Th2 cells and mast cells,leading enhanced cytokine production and eosinophil infiltration,consequently resulting in the development and/or aggravation of AD.IL-33 can affect impaired epidermal barrier,leading to repetitive cycle of barrier dysfunction and pruritus.In order to further explore the molecular mechanisms of AD and strategies of new drug usage,it is an urgent need to improve the therapeutic efficacy of AD.This article aims to summarize the important role of IL-33 in the pathogenesis and development of AD in multiple aspects.