摘要
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、CXCL10等细胞因子可能会诱发和加重银屑病。
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 keratinoeytes 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 keratino- cytes 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.
出处
《国际免疫学杂志》
CAS
北大核心
2010年第1期42-44,共3页
International Journal of Immunology