摘要
目的观察IFN γ能否在正常皮肤诱导表达银屑病皮损的病理表型 ,以及这一过程中IFN γ和表皮内源性白细胞介素 1(IL 1)系统的相互影响。方法采用跨膜器官培养和多种细胞因子刺激培养的皮肤 ,用免疫染色方法分析比较一系列代表银屑病免疫病理特征的多种蛋白分子的表达情况。结果IFN γ可诱导培养的正常皮肤表达角蛋白17 ,I型转谷酰胺酶(transglutaminasetypeI) ,细胞间粘附分子 1(ICAM 1)和HLA DR。IL 1受体拮抗剂(IL lra)或抗IL 1抗体 ,均可显著抑制IFN γ诱导的角蛋白17和I型转谷酰胺酶表达 ,而对IFN γ诱导ICAM 1和HLA DR的表达则无抑制作用。结论IFN γ可诱导人正常皮肤表达银屑病皮损的免疫病理表型 ,其中对角蛋白17和I型转谷酰胺酶的表达可通过表皮IL 1系统发挥影响。这项研究揭示 ,Th1型细胞因子(IFN γ)和表皮IL 1系统在银屑病皮损形成中具有内在的联系。
Aim The biological role of IFN γin the induction of the psoriatic phenotype expression and its interaction with epidermal IL 1 system was investigated in a skin organ culture model. Methods The tissue biopsies from healthy human skin were cultured for 24 hours and stimulated with IFN γ, IL 1 receptor antagonist(IL lra),IFN γ plus IL 1ra or anti IL 1 antibodies. The induction of the epidermal psoriatic phenotype expression was analysed by immunostaining (APAAP). Results In the presence of IFN γ, a strong upregulation of keratin 17 and transglutaminase type I(Tg type I) was found in the suprabasal layers of cultured normal skin. The ICAM 1 and HLA DR were expressed on basal and suprabasal keratinocytes. Addition of IL 1ra or anti IL 1 polyclonal antibodies into the IFN γ con taining medium could selectively block the effects of IFN γ on the expressions of keratin 17 and transglutaminase type I, but no effects on IFN γ induced expressions of ICAM 1 and HLA DR were discovered. Conclusion IFN γ is able to induce an immunopathologic phenotype of psoriasis in cultured normal human skin and this induction is partially via the epidermal IL 1 system. Above results suggested that there is an important intrinsic connection between Th1 cytokines and the IL 1 system, and they were two crucial factors in the pathogenesis of psoriasis.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
2000年第2期142-145,共4页
Chinese Journal of Cellular and Molecular Immunology
关键词
银屑病
Γ-干扰素
白细胞介素1
psoriasis
interferon γ
interleukin 1
skin organ culture
