CAJ | 학술논문

银屑病的发病机制主要表现为以T细胞介导的以角质形成细胞(KC)为靶点的免疫应答反应.在T细胞因子作用下,KC可能会出现异常的增殖和分化,其通过表达细胞因子参与T细胞的记忆和活化.Th17细胞是一种新发现的CD4~+T细胞亚群,因其分泌IL-17(IL-17A)而命名.IL-17促进KC产生VEGF、IL-8、GM-CSF、TNF-α、CXCL1O等细胞因子可能会诱发和加重银屑病.
은설병적발병궤제주요표현위이T세포개도적이각질형성세포(KC)위파점적면역응답반응.재T세포인자작용하,KC가능회출현이상적증식화분화,기통과표체세포인자삼여T세포적기억화활화.Th17세포시일충신발현적CD4~+T세포아군,인기분비IL-17(IL-17A)이명명.IL-17촉진KC산생VEGF、IL-8、GM-CSF、TNF-α、CXCL1O등세포인자가능회유발화가중은설병.
The pathogenesis of psoriasis is considered as a kind of T cell-mediated immune response resulting in the hyperproliferation and differentiation of epidermal keratinocytes (KC), and the cytokines expressed by keratinocytes take part in the activation of T cells. Recent studies show that Th17 cells are a newly discovered CD4~+ T helper cell subset which can secrete interleukin-17 (IL-17A). IL-17 can stimulate keratinocytes to produce cytokines including vascular endothelial growth factor (VEGF), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor alpha (TNF-α), and chemokine (C-X-C motif) lig-and 10 (CXCL10). These cytokines may play important roles in the development or aggravation of psoriasis.