Leung D Y
National Jewish Center for Immunology and Respiratory Medicine, Department of Pediatrics, University of Colorado Health Sciences Center, Denver 80206, USA.
Clin Exp Immunol. 1997 Jan;107 Suppl 1:25-30.
Atopic dermatitis (AD), a chronic inflammatory skin disease, is frequently seen in patients with a personal or family history of asthma and allergic rhinitis. Population studies suggest an increasing prevalence of AD in children since World War II, with 10-15% of the population being affected by AD at some time during childhood. In patients with moderate to severe AD, involvement can be life-long, causing significant interference with school, work and social interactions. The term atopic dermatitis was introduced to reflect the close association between AD and respiratory allergy. During the past decade, extraordinary progress has been made in our understanding of the immunopathogenesis of allergic diseases. In particular, this constellation of inherited illnesses has now been demonstrated to be associated with activation of a specific group of cytokine genes encompassing IL-3, IL-4, IL-5, IL-13 and granulocyte-macrophage colony-stimulating factor (GM-CSF). The molecular basis for selective activation of this cytokine gene cluster and the immunological consequences are now being pursued actively by many laboratories. However, it is clear that allergic diseases result from a polygenic inheritance pattern which involves not only cytokine gene activation but also activation of other less well defined gene products. Furthermore, the clinical expression of allergic diseases is highly dependent on a complex interaction between the host and its environment, e.g. allergen exposure. The genetic predisposition to develop allergic responses may be similar in patients with AD and other allergic diseases, such as asthma. However, targeting of the allergic immune response may relate to the organ in which allergen sensitization first occurs; the capacity of immune effector cells, e.g. T lymphocytes, to home preferentially to the skin versus the respiratory mucosa; and the programmed response of resident cells, e.g. epithelial cells, to injury and inflammation. This review examines the cellular and immunological mechanisms that are thought to play an important role in the pathogenesis of chronic AD. An understanding of the immunological basis of AD is likely to have important clinical implications in our approach to the management of this common illness, and the development of immunomodulators for its treatment.
特应性皮炎（AD）是一种慢性炎症性皮肤病，常见于有个人或家族哮喘及过敏性鼻炎病史的患者。人群研究表明，自第二次世界大战以来，儿童AD的患病率呈上升趋势，10% - 15%的人口在童年时期的某个阶段会受到AD影响。在中重度AD患者中，病情可能会持续一生，对学习、工作和社交互动造成严重干扰。引入“特应性皮炎”这一术语是为了反映AD与呼吸道过敏之间的密切关联。在过去十年中，我们对过敏性疾病的免疫发病机制的理解取得了非凡进展。特别是，现已证明这一系列遗传性疾病与一组特定的细胞因子基因的激活有关，这些基因包括白细胞介素 - 3（IL - 3）、白细胞介素 - 4（IL - 4）、白细胞介素 - 5（IL - 5）、白细胞介素 - 13（IL - 13）和粒细胞 - 巨噬细胞集落刺激因子（GM - CSF）。许多实验室正在积极研究该细胞因子基因簇选择性激活的分子基础及其免疫学后果。然而，很明显过敏性疾病是由多基因遗传模式导致的，这不仅涉及细胞因子基因的激活，还涉及其他定义不太明确的基因产物的激活。此外，过敏性疾病的临床表现在很大程度上取决于宿主与其环境之间的复杂相互作用，例如接触过敏原。AD患者和其他过敏性疾病（如哮喘）患者发生过敏反应的遗传易感性可能相似。然而，针对过敏性免疫反应可能与过敏原致敏首先发生的器官有关；免疫效应细胞（如T淋巴细胞）优先归巢至皮肤而非呼吸道黏膜的能力；以及驻留细胞（如上皮细胞）对损伤和炎症的程序性反应。本综述探讨了被认为在慢性AD发病机制中起重要作用的细胞和免疫机制。了解AD的免疫学基础可能对我们治疗这种常见疾病的方法以及开发其免疫调节剂具有重要的临床意义。
