Schöpf E, Kapp A
Immun Infekt. 1985 Sep;13(5):179-83.
Atopic dermatitis (AD) is a familial inflammatory skin disorder which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing time course and the personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis). However, there exists a variety of additional features which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, the pathogenesis is not clearly understood at present. This review summarizes the reported deviations of the immune system as well as the alterations of the mediators of inflammation and the abnormalities of cyclic nucleotide regulation. These findings will be correlated with clinical symptoms. In particular the following topics were taken into consideration: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation and especially the observations on the cyclic adenosine monophosphate (cAMP)-phosphodiesterase. These extremely complex findings based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system may provide a better understanding of the pathogenesis of atopic dermatitis.
特应性皮炎（AD）是一种家族性炎症性皮肤病，其特征为剧烈瘙痒、典型的形态和分布、慢性或慢性复发性病程以及个人或家族的特应性病史（哮喘、过敏性鼻炎、特应性皮炎）。然而，还存在多种其他特征，这些特征要么特异性较低，要么相对罕见。尽管这种疾病自本世纪初就已为人所知，但目前其发病机制尚不清楚。本综述总结了所报道的免疫系统偏差、炎症介质的改变以及环核苷酸调节异常。这些发现将与临床症状相关联。特别考虑了以下主题：与HLA抗原的关联、血清IgE升高和IgE免疫复合物的产生、T抑制细胞的数量和功能缺陷、粒细胞的参与、炎症介质的改变，尤其是对环磷酸腺苷（cAMP）磷酸二酯酶的观察。基于自主神经系统失调与免疫系统改变之间相互作用的这些极其复杂的发现，可能有助于更好地理解特应性皮炎的发病机制。
