银屑病
炎症
免疫系统
免疫学
疾病
表观遗传学
白细胞介素17
肿瘤坏死因子α
医学
病理
生物
遗传学
基因
作者
Daniel Sortebech,Trine Schoenfeldt,Albert Duvetorp,Rasmus Agerholm,Liv Eidsmo
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2024-10-21
卷期号:213 (9): 1267-1277
标识
DOI:10.4049/jimmunol.2400020
摘要
Abstract The human skin forms a dynamic barrier to physical injuries and microbial invasion. Constant interactions between stroma and tissue-confined immune cells maintain skin homeostasis. However, the cellular interactions that maintain skin health also contribute to focal immunopathology. Psoriasis is a common disease that manifests with focal pathology induced by environmental triggers in genetically susceptible individuals. Within psoriasis plaques, cross-talk between skin-resident T cells and stroma cells leads to chronic inflammation. Inflammatory cytokines such as TNF-α, IL-17, IL-22, and IL-23 amplify the local chronic inflammation and sustain the well-demarcated thick and scaly plaques that characterize the disease. In resolved lesions, T cells remain poised for IL-17 and IL-22 production, and postinflammatory epigenetic modifications lower the threshold for initiation of local relapse. This review focuses on how tissue-resident memory T cells contribute to the onset, maintenance, resolution, and relapse of psoriasis.
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