文献类型：期刊文献

英文题名：A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis

作者：Zhou, Wenli[1];Li, Zhaoyu[2];Liu, Xuehai[3];Jia, Binkui[3];Pei, Xuedong[3];Wang, Di[4];Zhang, Haoling[4];Wang, Sinong[1]

第一作者：周文丽

通信作者：Wang, SN[1];Wang, D[2];Zhang, HL[2]

机构：[1]Gansu Univ Chinese Med, Affiliated Hosp, Sch Clin Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[4]Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, George Town 13200, Malaysia

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Affiliated Hosp, Sch Clin Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, George Town 13200, Malaysia.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2026

卷号：15

期号：3

起止页码：156

外文期刊名：AMERICAN JOURNAL OF CLINICAL AND EXPERIMENTAL IMMUNOLOGY

收录：WOS:【ESCI(收录号:WOS:001815888400001)】；

基金：The project title: Construction and Practice of the Theoretical System of "New Blood Syndrome Theory" for Psoriasis, Key Special Project of "Research on Modernization of Traditional Chinese Medicine" under the National Key Research and Development Program, 2023-ZD-219.

语种：英文

外文关键词：Psoriasis; immune inflammation; IL-23/Th17 axis; TNF-alpha; IL-17; immune cells; targeted therapy; preci-sion medicine; emerging targets

摘要：Psoriasis is a chronic immune-mediated inflammatory skin disease caused by dysregulated interaction between innate and adaptive immune cells. Of note, the IL-23/Th17 axiom is new central circuit amongst known pathways, while TNF-alpha, IL-17 family cytokines and IL-36 mediate the dysfunction of keratinocyte and tissue in inflammation. An interconnecting inflammatory network involves dendritic cells, T-cell populations, keratinocytes, neutrophils and fibroblasts that plate epidermal hyperproliferation and lesional immune-cell recruitment. Biologics targeting TNF-alpha and IL-17 and IL-23 are clinically transformative in the treatment of disease, but a large cohort of patients are left with incomplete response, resistance or challenges in long-term management. Other novel targets such IL-36R and AHR may extend the window of therapeutic opportunity. Molecular stratification and biomarker-driven treatment selection also merit investigation in parallel with further delineation of a specific therapeutic strategy.