Terui Tadashi
Department of Dermatology, Nihon University School of Medicine, Japan.
J Pharmacol Sci. 2009 Jul;110(3):232-6. doi: 10.1254/jphs.09r02fm.
It has been recognized that atopic dermatitis (AD) involves allergen-driven Th2 cell polarization. In patients with AD, cytokines induce allergic inflammatory responses and subsequently enhance IgE production. Recent reports revealed that a reduced barrier function as well as altered immunity are fundamental to the development of AD because barrier disruption due to aberrant filaggrin expression is a pathological factor. However, although recent studies have improved our understanding of the pathogenesis of AD, the overall pathophysiology remains elusive. I herein discuss it based on the natural history of AD.
人们已经认识到,特应性皮炎(AD)涉及过敏原驱动的Th2细胞极化。在AD患者中,细胞因子诱导过敏性炎症反应,随后增强IgE的产生。最近的报告显示,屏障功能降低以及免疫改变是AD发病的基础,因为异常丝聚合蛋白表达导致的屏障破坏是一个病理因素。然而,尽管最近的研究增进了我们对AD发病机制的理解,但整体病理生理学仍不明确。我在此根据AD的自然病史进行讨论。