贾纳斯激酶
STAT蛋白
鲁索利替尼
斯达
医学
JAK-STAT信号通路
胸腺基质淋巴细胞生成素
特应性皮炎
免疫学
发病机制
信号转导
车站3
STAT6
免疫系统
刺猬信号通路
细胞因子
癌症研究
白细胞介素4
生物
酪氨酸激酶
受体
内科学
骨髓
生物化学
骨髓纤维化
作者
I‐Hsin Huang,Yi‐Teng Hung,Po‐Chien Wu,Chun‐Bing Chen
标识
DOI:10.3389/fimmu.2022.1068260
摘要
Atopic dermatitis (AD) is a chronic, inflammatory, pruritic form of dermatosis with heterogeneous manifestations that can substantially affect patients' quality of life. AD has a complex pathogenesis, making treatment challenging for dermatologists. The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway plays a central role in modulating multiple immune axes involved in the immunopathogenesis of AD. In particular, Th2 cytokines, including interleukin (IL)-4, IL-5, IL-13, IL-31, and thymic stromal lymphopoietin, which contribute to the symptoms of chronic inflammation and pruritus in AD, are mediated by JAK-STAT signal transduction. Furthermore, JAK-STAT is involved in the regulation of the epidermal barrier and the modulation of peripheral nerves related to the transduction of pruritus. Targeting the JAK-STAT pathway may attenuate these signals and show clinical efficacy through the suppression of various immune pathways associated with AD. Topical and oral JAK inhibitors with variable selectivity have emerged as promising therapeutic options for AD. Notably, topical ruxolitinib, oral upadacitinib, and oral abrocitinib were approved by the U.S. Food and Drug Administration for treating patients with AD. Accordingly, the present study reviewed the role of JAK-STAT pathways in the pathogenesis of AD and explored updated applications of JAK inhibitors in treating AD.
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