Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Leo Foundation Skin Immunology Research Center, University of Copenhagen, Copenhagen, Denmark.
J Immunol. 2024 Nov 1;213(9):1267-1277. doi: 10.4049/jimmunol.2400020.
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.
人类皮肤形成了一道动态的屏障，防止物理损伤和微生物入侵。基质与组织受限的免疫细胞之间的持续相互作用维持着皮肤的稳态。然而，维持皮肤健康的细胞相互作用也导致了局部免疫病理学。银屑病是一种常见的疾病，表现为遗传易感个体在环境诱因作用下出现局灶性病理改变。在银屑病斑块中，皮肤驻留 T 细胞与基质细胞之间的相互作用导致慢性炎症。TNF-α、IL-17、IL-22 和 IL-23 等炎症细胞因子放大局部慢性炎症，并维持特征性疾病的明显界限增厚和鳞屑斑块。在已解决的病变中，T 细胞仍然能够产生 IL-17 和 IL-22，炎症后的表观遗传修饰降低了局部复发的起始阈值。这篇综述重点讨论了组织驻留记忆 T 细胞如何导致银屑病的发病、维持、缓解和复发。
