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首页> 外文期刊>International immunopharmacology >D-pinitol inhibits Th1 polarization via the suppression of dendritic cells.
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D-pinitol inhibits Th1 polarization via the suppression of dendritic cells.

机译：D-松醇通过抑制树突状细胞来抑制Th1极化。

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d-pinitol has been demonstrated to exert insulin-like and anti-inflammatory effects. However, the effects of the maturation and immunostimulatory functions of dendritic cells (DC) remain to be clearly elucidated. In this study, we have attempted to determine whether d-pinitol regulates surface molecule expression, cytokine production, endocytosis capacity, and underlying signaling pathways in murine bone marrow-derived DC. We also attempted to ascertain whether d-pinitol could influence Th1/Th2 immune response in vivo. The DC used in this study were derived from murine bone marrow cells, and were used as immature or LPS-stimulated mature DC. The DC were then assessed with regard to surface molecule expression, dextran-FITC uptake, cytokine production, capacity to induce T-cell differentiation, and underlying signaling pathways. d-pinitol was shown to significantly inhibit CD80, CD86, MHC class I, and MHC class II expression in the LPS-stimulated mature DC. The DC also evidenced impaired IL-12 expression and IFN-gamma production. The d-pinitol-treated DC were found to be highly efficient in regards to Ag capture via mannose receptor-mediated endocytosis. d-pinitol was also demonstrated to inhibit LPS-induced MAPKs activation and NF-kappaB nuclear translocation. Moreover, the d-pinitol-treated DC manifested impaired induction of Th1 responses, and normal cell-mediated immune responses. These novel findings provide new insight into the immunopharmacological role of d-pinitol in terms of its effects on DC. These findings also broaden current perspectives concerning our understanding of the immunopharmacological functions of d-pinitol, and have ramifications for the development of therapeutic adjuvants for the treatment of DC-related acute and chronic diseases.
机译：d-松醇已被证明具有胰岛素样和抗炎作用。但是，树突状细胞（DC）的成熟和免疫刺激功能的影响仍有待阐明。在这项研究中，我们试图确定d-松醇是否调节鼠骨髓来源的DC中的表面分子表达，细胞因子产生，内吞能力和潜在的信号通路。我们还试图确定d-松醇是否可以在体内影响Th1 / Th2免疫反应。本研究中使用的DC来源于鼠骨髓细胞，并用作未成熟或LPS刺激的成熟DC。然后评估DC的表面分子表达，右旋糖酐FITC摄取，细胞因子产生，诱导T细胞分化的能力和潜在的信号通路。 d-松醇显示在LPS刺激的成熟DC中显着抑制CD80，CD86，I类MHC和II类MHC表达。 DC还证明IL-12表达和IFN-γ产生受损。发现经d-松醇处理的DC对于通过甘露糖受体介导的内吞作用捕获Ag是高效的。还证明了d-松醇可抑制LPS诱导的MAPKs活化和NF-kappaB核易位。此外，经d-松醇治疗的DC表现出Th1应答诱导和正常细胞介导的免疫应答受损。这些新发现提供了关于d-松醇对DC的免疫药理作用的新见解。这些发现也拓宽了有关我们对D-松醇的免疫药理功能理解的观点，并为开发治疗DC相关的急性和慢性疾病的治疗佐剂产生了影响。

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