摘要
Triptolide is a natural, biologically active component derived from Chinese herb Tripterygium Wilfordii Hook F. (TWHF) which is effective in the clinical treatment of autoimmune diseases, however, the mechanisms by which triptolide exerts immunosuppression remain fully understood. The primary of this study is to demonstrate whether triptolide can affect phenotype, cytokine production and allogeneic T cell-stimulatory capacity of dendritic cells (DCs) which are critical in the induction of immune response or tolerance. Phenotypic analysis show that triptolide does not affect the expression of MHC (Ia b), CD80, CD86 and CD40 of DC stimulated with or not LPS, but significantly inhibits IL-12p70 production by DC in a dose-dependent manner. Triptolide-treated DCs exhibit a reduced capacity to stimulate proliferation of allogeneic CD4 + T lymphocytes. Therefore, triptolide-mediated immunosuppression may due, in part, to the inhibition of IL-12p70 production and impairment of allogeneic T cell-stimulatory capacity of DCs. Our results may provide a possible mechanistic explanation for the effectiveness of triptolide in the treatment of autoimmune diseases.
Triptolide is a natural, biologically active component derived from Chinese herb Tripterygium Wilfordii Hook F. (TWHF) which is effective in the clinical treatment of autoimmune diseases, however, the mechanisms by which triptolide exerts immunosuppression remain fully understood. The primary of this study is to demonstrate whether triptolide can affect phenotype, cytokine production and allogeneic T cell-stimulatory capacity of dendritic cells (DCs) which are critical in the induction of immune response or tolerance. Phenotypic analysis show that triptolide does not affect the expression of MHC (Ia b), CD80, CD86 and CD40 of DC stimulated with or not LPS, but significantly inhibits IL-12p70 production by DC in a dose-dependent manner. Triptolide-treated DCs exhibit a reduced capacity to stimulate proliferation of allogeneic CD4 + T lymphocytes. Therefore, triptolide-mediated immunosuppression may due, in part, to the inhibition of IL-12p70 production and impairment of allogeneic T cell-stimulatory capacity of DCs. Our results may provide a possible mechanistic explanation for the effectiveness of triptolide in the treatment of autoimmune diseases.
