特应性皮炎的发病机制及其治疗现状

Current research on pathogenesis and treatment of atopic dermatitis

特应性皮炎（AD）是一种有遗传倾向的过敏性疾病，发病机制复杂，主要与遗传背景、环境刺激、表皮屏障缺陷、免疫失调等因素有关。表皮屏障的破坏刺激炎症反应，急性期Th21细胞活化，产生IL4等细胞因子诱导B细胞产生IgE，导致肥大细胞、嗜碱性粒细胞脱颗粒。急性期后表皮增厚，神经纤维增生，趋化因子表达增加。慢性期时包含Th2细胞和Th1细胞，Th17和Th22细胞浸润。后两种细胞与成纤维细胞和角质细胞来源的趋化因子和细胞因子共同驱动组织重塑和纤维化。目前对AD的治疗主要是避免接触过敏原，局部或系统抗炎抗感染，光疗，免疫治疗等。

Atopic dermatitis （AD） is an allergic skin disease with a genetic predisposition. The pathogenesis is complex, including environment stimulation, epidermal barrier deficiency, and autoimmune disorders. The destruction of epidermal barrier stimulates the inflammatory response. In acute period, Th2 ceils are activated to produce IL-4 and induce B lymphocytes to secrete IgE. Thus leads to degranulation of mast cells and basophils. After acute period, epidermis is thickened, accompanied with increasing expression levels of several chemokines and cytokines. In chronic phase, the cellular infiltration includes mainly Thl and Th2 cells, and less Th17 and Th22 cells. The latter two cells together with their specific cytokines and chemokines are derived from keratinocytes and fibroblasts, which can produce tissue remodeling and fibrosis. So far, the treatment of AD contains allergens exposure avoid, anti-inflammatory, anti-infection, phototherapy, and immune therapy, etc.