特应性皮炎
免疫学
脱颗粒
发病机制
趋化因子
免疫系统
医学
银屑病
免疫球蛋白E
表皮(动物学)
过敏
抗体
解剖
内科学
受体
作者
Tao Huang,Yunsheng Liang
出处
期刊:Journal of Chinese Physician
日期:2016-02-20
卷期号:18 (2): 161-164
标识
DOI:10.3760/cma.j.issn.1008-1372.2016.02.001
摘要
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 cells 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 Th1 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.
Key words:
Dermatitis, atopic/ET/TH; Editorial
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