Bao Lei, Zhang Huayi, Chan Lawrence S
Department of Dermatology; University of Illinois; Chicago, IL USA.
JAKSTAT. 2013 Jul 1;2(3):e24137. doi: 10.4161/jkst.24137. Epub 2013 Aug 15.
Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by inflammatory cell skin infiltration. The JAK-STAT pathway has been shown to play an essential role in the dysregulation of immune responses in AD, including the exaggeration of Th2 cell response, the activation of eosinophils, the maturation of B cells, and the suppression of regulatory T cells (Tregs). In addition, the JAK-STAT pathway, activated by IL-4, also plays a critical role in the pathogenesis of AD by upregulating epidermal chemokines, pro-inflammatroy cytokines, and pro-angiogenic factors as well as by downregulating antimicrobial peptides (AMPs) and factors responsible for skin barrier function. In this review, we will highlight the recent advances in our understanding of the JAK-STAT pathway in the pathogenesis of AD.
特应性皮炎（AD）是一种常见的慢性炎症性皮肤病，其特征为炎症细胞浸润皮肤。研究表明，JAK-STAT信号通路在AD免疫反应失调中起关键作用，包括Th2细胞反应过度、嗜酸性粒细胞活化、B细胞成熟以及调节性T细胞（Tregs）受抑制。此外，由白细胞介素-4激活的JAK-STAT信号通路，通过上调表皮趋化因子、促炎细胞因子和促血管生成因子，以及下调抗菌肽（AMPs）和负责皮肤屏障功能的因子，在AD发病机制中也起着关键作用。在本综述中，我们将重点介绍对JAK-STAT信号通路在AD发病机制中的理解的最新进展。
