变应性接触性皮炎的免疫机制

摘要

Allergic contact dermatitis ( ACD) is a delayed-type hypersensitivity which is mediated by hapten-specific T cell.The pathogenesis of ACD is divided into sensitization and elicitation phases.The first contact of skin with haptens lead to binding of the hapten to endogenous proteins in skin, forming immunogenic hapten-carrier complexes in sensitization phase.The hapten-carrier complex is captured by antigen-presenting cells ( APCs) , which migrate from the epidermis to lymph node.The haptenated peptides is presented to naive T cells which are activated subsequently.The newly activated T cells proliferate and migrate into circulation from the lymph node.Re-exposure of the skin to the hapten activates the specific T cells in the dermis and produces various chemical mediators, which induce antigen-specific inflammation in elicitation phase.Molecular and cellular pathways in the pathogenesis of ACD, progress and novel knowledge of other cell such as B1 cells, natural killer ( NK) T cells and NK cells involved in ACD were summarized, while the characteristics of the mouse dermatitis models was also summarized in this review.%变应性接触性皮炎（allergic contact dermatitis， ACD）是由半抗原-特异性T细胞介导、在过敏原接触皮肤后激发产生的迟发型超敏反应（Ⅳ型超敏反应），包含致敏期和激发期。在致敏阶段，半抗原和皮肤中的内源性蛋白组成具有免疫性的抗原蛋白复合体，复合体被抗原提呈细胞（ antigen presenting cells， APCs）捕获后，随APCs从表皮迁移至淋巴结。随后，抗原蛋白复合体活化初始T细胞。活化的T细胞在淋巴结中增殖并分化成为抗原特异性效应T细胞并迁移至循环中。在激发阶段，效应T细胞被皮肤中的APCs再次激活，分泌多种化学介质并引起抗原特异性炎症反应。本文介绍ACD发展过程中的分子和细胞通路以及机制研究的新进展，探索肥大细胞、 B细胞、自然杀伤T细胞和自然杀伤细胞等在ACD发展过程中的作用。并对现已建立的动物模型进行总结，讨论其特点和运用。