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Cytokine expression in three mouse models of experimental hepatitis.

机译:在实验性肝炎的三种小鼠模型中细胞因子的表达。

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摘要

The activation of T-cells and macrophages and subsequent induction of cytokines are critical factors in the development of hepatitis. Up-regulation of pro-inflammatory cytokines, e.g. TNF has been shown to induce liver injury while counter regulation by anti-inflammatory cytokines, e.g. IL-10 is protective. We compared the induction of liver injury and the expression pattern of a variety of cytokines in T-cell- versus non-T-cell-dependent mouse models of liver injury. TNF, IFNgamma, IL-2, IL-4, IL-6, IL-10 and IL-12 were measured in plasma and liver tissue after either Concanavalin A (Con A), D-galactosamine/lipopolysaccharide (GalN/LPS) or high dose LPS induced liver injury. Additionally, the intra-hepatic expression of the putative pathogenicity factor high mobility group 1 protein (HMG-1) was compared in all three models.
机译:T细胞和巨噬细胞的激活以及随后的细胞因子诱导是肝炎发展的关键因素。促炎细胞因子的上调,例如TNF已显示出诱导肝损伤,同时通过抗炎细胞因子例如β-内啡肽反调节。 IL-10具有保护作用。我们比较了肝损伤的T细胞依赖性和非T细胞依赖性小鼠模型中肝损伤的诱导和多种细胞因子的表达模式。在伴刀豆球蛋白A(Con A),D-半乳糖胺/脂多糖(GalN / LPS)或血浆中检测血浆和肝组织中的TNF,IFNgamma,IL-2,IL-4,IL-6,IL-10和IL-12大剂量脂多糖引起肝损伤。此外,在所有三个模型中比较了假定的致病性因子高迁移率第1组蛋白(HMG-1)在肝内的表达。

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