医学
联合疗法
下调和上调
银屑病
免疫系统
癌症研究
特应性皮炎
PI3K/AKT/mTOR通路
C-C趋化因子受体7型
炎症
免疫学
药理学
角质形成细胞
信号转导
治疗方法
促炎细胞因子
趋化性
树突状细胞
作者
YaMei Gao,Xueting Shen,JiLiang Lu,ChaoJing Zhou,Shaohu Huo,ZiYue Diao,Chao Chen,Xin Han,Zhiqiang Yin
标识
DOI:10.1186/s12951-026-04637-2
摘要
Inflammatory skin diseases (ISDs) pose a major global burden, yet current therapies are limited by efficacy, accessibility, and cost, necessitating novel effective treatments. Thus, our study proposes a novel synergistic therapeutic strategy for psoriasis (PSO) and atopic dermatitis (AD) by concurrently targeting two critical pathological axes: immune cell chemotaxis via CCR7 inhibition and local inflammatory signaling via JAK1 suppression. A pH-responsive hydrogel (C-P@U/C-siCCR7) was designed for co-delivery of CCR7-targeting siRNA and the JAK1 inhibitor upadacitinib (UPA). Multi-omics analysis confirmed specific CCR7 overexpression in patient and model tissues. In vitro, the system inhibited keratinocyte proliferation, induced apoptosis, and downregulated key proteins in the JAK-STAT and PI3K/AKT/mTOR pathways along with pro-inflammatory cytokines. In IMQ-induced PSO and DNCB-induced AD mouse models, topical hydrogel application ameliorated skin lesions, restored the epidermal barrier, reduced hyperplasia and infiltration, and alleviated systemic immune activation-including suppression of splenomegaly and serum cytokines (IL17A, TNFα, IL4, IL13)-with favorable biosafety. The therapeutic effects were mechanistically linked to synergistic downregulation of CCR7, JAK1, STAT3, and mTOR in lesions, and reduced populations of aberrantly activated T cells, neutrophils, and dendritic cells in the spleen. This work provides a novel delivery platform and experimental evidence for developing effective, precise topical combination therapies against ISDs.
科研通智能强力驱动
Strongly Powered by AbleSci AI