节点文献

白介素-1β诱导正常人皮肤表达银屑病免疫病理表型

IL-1βInduces Psoriatic Phenotype in Cultured Normal Human Skin

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 刘玮赵庆利Reno Debets蔡瑞康Errol P Prens

【Author】 LIU Wei, ZHAO Qingli, R.Debets, et al. Department of Dermatology, The General Hospital of Air Force, Beijing 100036

【机构】 空军总医院皮肤科荷兰Erasmus大学医学院免疫系免疫皮肤病研究室

【摘要】 目的对白介素 -1β(IL 1β)在启动银屑病免疫病理表型中的作用进行研究。方法取健康人正常皮肤在跨膜(transwell)皮肤器官培养模型中进行培养 ,观察在IL 1β或白介素 -1受体拮抗剂(IL 1ra)等细胞因子刺激下 ,培养皮肤表达银屑病免疫病理特征标记物的情况。结果在IL 1β 刺激下 ,正常人皮肤表达了一系列银屑病相关的蛋白分子 ,即角蛋白16、17在表皮棘细胞层强阳性 ;Ⅰ型转谷酰胺酶从表皮颗粒层到棘细胞层过度表达 ;ICAM 1、HLA DR以及β1整合素在表皮基底细胞层和棘细胞层诱导表达或增强表达。培养基中加入IL 1ra可使上述标记物的表达受到显著抑制。培养基中加入抗IL 1β抗体可完全阻断IL 1β的上述诱导作用。结论在培养条件下IL 1β可诱导正常人皮肤表达银屑病的免疫病理表型 ,提示IL 1系统参与了银屑病的皮损形成。

【Abstract】 Objective To investigate the role of IL 1βin the initiation of psoriatic phenotype in the transwell skin organ culture model using biopsies from healthy human skin and non lesional skin from patients with psoriasis. Methods The skin biopsies were cultured for 24 hours and stimulated with IL 1βor IL 1 receptor antagonist (IL 1ra), and the induction of epidermal psoriatic phenotype was analysed using immunostaining (APAAP). Results In the presence of IL 1β, the psoriasiform epidermal phenotype was clearly induced, i.e. a strong upregulation of keratin 16, keratin 17 and transglutaminase type Ⅰwas found in the suprabasal layers of cultured normal skin; the expression of ICAM 1 and HLA DR was induced on basal keratinocytes, epidermal dendritic cells as well as endothelial cells in the dermis. Integrin β1 was also upregulated by IL 1βfrom the basal to suprabasal keratinocytes. The effects of IL 1βon the skin organ cultures could be completely neutralized by anti IL 1 polyclonal antibodies. Conclusion IL 1βis able to induce a series of psoriasis related markers in cultured normal human skin, which suggests that IL 1 be involved in the initiation of psoriasis.

【关键词】 银屑病白细胞介素-1细胞因子
【Key words】 Psoriasis Interleukin 1 Cytokine
  • 【文献出处】 中华皮肤科杂志 ,CHINESE JOURNAL OF DERMATOLOGY , 编辑部邮箱 ,1999年02期
  • 【分类号】R758.63
  • 【被引频次】12
  • 【下载频次】126
节点文献中: 

本文链接的文献网络图示:

本文的引文网络