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首页> 外文期刊>Allergy >Effector and regulatory mechanisms in allergic contact dermatitis.
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Effector and regulatory mechanisms in allergic contact dermatitis.

机译：过敏性接触性皮炎的效应子和调节机制。

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摘要

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.
机译：过敏性接触性皮炎（ACD）是最常见的职业病之一，是由T细胞介导的皮肤炎症，是由反复接触皮肤接触过敏原（即称为半抗原的非蛋白质化学物质）引起的。过敏性接触性皮炎，也称为接触性超敏反应，是由CD8 + T细胞介导的，CD8 + T细胞在敏化阶段在淋巴器官中引发，并在再次暴露于半抗原后募集到皮肤中。具有抑制活性的CD4 + T细胞亚群既可导致过敏性患者湿疹的下调，又可防止非过敏性个体向半抗原致敏。因此，应将ACD视为对半抗原的皮肤免疫耐受性的细分。 ACD病理生理学的最新进展证明了皮肤先天免疫在敏化过程中的重要作用，并重新认识到朗格汉斯细胞是CD8 + T细胞启动所必需的教条。他们还引入了肥大细胞，作为炎症反应程度的关键因素。最后，最近的研究针对控制皮肤炎症的调节性T细胞的性质，模式和作用部位，目的是开发过敏性患者中诱导耐受性的新策略。

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