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变应性接触性皮炎中的效应器和调节机制。

Effector and regulatory mechanisms in allergic contact dermatitis.

机构信息

Faculté de Médecine Lyon Sud, Université Lyon1, Lyon, France.

出版信息

Allergy. 2009 Dec;64(12):1699-714. doi: 10.1111/j.1398-9995.2009.02082.x. Epub 2009 Oct 12.

DOI:10.1111/j.1398-9995.2009.02082.x
PMID:19839974
Abstract

Allergic contact dermatitis (ACD), one of the commonest occupational diseases, is a T-cell-mediated skin inflammation caused by repeated skin exposure to contact allergens, i.e. nonprotein chemicals called haptens. Allergic contact dermatitis, also referred to as contact hypersensitivity, is mediated by CD8+ T cells, which are primed in lymphoid organs during the sensitization phase and are recruited in the skin upon re-exposure to the hapten. Subsets of CD4+ T cells endowed with suppressive activity are responsible for both the down-regulation of eczema in allergic patients and the prevention of priming to haptens in nonallergic individuals. Therefore, ACD should be considered as a breakdown of the skin immune tolerance to haptens. Recent advances in the pathophysiology of ACD have demonstrated the important role of skin innate immunity in the sensitization process and have revisited the dogma that Langerhans cells are mandatory for CD8+ T-cell priming. They have also introduced mast cells as a pivotal actor in the magnitude of the inflammatory reaction. Finally, the most recent studies address the nature, the mode and the site of action of the regulatory T cells that control the skin inflammation with the aim of developing new strategies of tolerance induction in allergic patients.

摘要

变应性接触性皮炎(ACD)是最常见的职业病之一,是一种由接触过敏原(即非蛋白质化学物质称为半抗原)反复引起的 T 细胞介导的皮肤炎症。变应性接触性皮炎,也称为接触超敏反应,是由 CD8+T 细胞介导的,这些细胞在致敏阶段在淋巴器官中被激活,并在重新暴露于半抗原时在皮肤中募集。具有抑制活性的 CD4+T 细胞亚群负责调节过敏性患者的湿疹,并防止非过敏性个体对半抗原的致敏。因此,ACD 应被视为皮肤对半抗原的免疫耐受的破坏。ACD 的发病机制的最新进展表明皮肤固有免疫在致敏过程中的重要作用,并重新审视了朗格汉斯细胞对半抗原 CD8+T 细胞启动是必需的这一观点。它们还将肥大细胞作为炎症反应程度的关键因素引入。最后,最近的研究探讨了调节性 T 细胞的性质、作用方式和作用部位,以控制皮肤炎症,旨在为过敏性患者开发新的诱导耐受策略。

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Effector and regulatory mechanisms in allergic contact dermatitis.变应性接触性皮炎中的效应器和调节机制。
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