摘要
无菌性脓疱病的发病机制涉及多种细胞及炎症因子。在外界刺激下,角质形成细胞通过CCL20/CCR6系统、C5a分别趋化T淋巴细胞和中性粒细胞。T淋巴细胞通过穿孔素/颗粒酶B系统和Fas/FasL系统促进表皮内水疱形成,表达CXCL8趋化中性粒细胞、促进角质形成细胞提呈抗原。同时,激活的中性粒细胞可以表达人白细胞DR抗原,刺激T细胞,放大炎症。另外,局部或全身皮肤抗白细胞蛋白酶水平降低也促进脓疱的形成。
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.
出处
《国际皮肤性病学杂志》
2007年第5期287-289,共3页
International Journal of Dermatology and Venereology
