发病机制
免疫学
20立方厘米
穿孔素
颗粒酶
抗原
炎症
免疫系统
趋化因子
生物
医学
CD8型
趋化因子受体
摘要
The pathogenesis of sterile pustulosis involves various cells and inflammatory mediators. Upon outside stimulation, keratinocytes induce the accumulation of T lymphocytes and neutrophils respectively by CCL20/CCR6 system and peptide C 5a . T lymphocytes not only facilitate the formation of intraepidermal vesicles by the perforin/granzyme B and Fas/Fasl system, but also produce CXCL8 to enhance the recruitment of neutrophils and antigen presentation of keratinocytes. Meanwhile, activated neutrophils could express human leukocyte antigen (HLA) -DR and excite T lymphocytes to amplify the inflammation. Besides, the decrease of local or systemic levels of skin-derived antileukoproteinase also contributes to the formation of pustules.
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