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首页> 外文期刊>Cellular immunology >Paclitaxel enhances early dendritic cell maturation and function through TLR4 signaling in mice.
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Paclitaxel enhances early dendritic cell maturation and function through TLR4 signaling in mice.

机译：紫杉醇通过TLR4信号转导小鼠增强树突状细胞的早期成熟和功能。

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摘要

Subclinical doses of Paclitaxel (PTX) given 1day prior to a HER-2eu (neu)-targeted, granulocyte-macrophage colony stimulating factor (GM-CSF)-secreting whole-cell vaccine enhances neu-specific T cell responses and slows neu(+) tumor growth in tolerized HER-2eu (neu-N) mice. We demonstrate that co-administration of PTX and Cyclophosphamide (CY) synergizes to slow tumor growth, and that in vitro, DC precursors exposed to PTX before LPS maturation results in greater co-stimulatory molecule expression, IL-12 production, and the ability to induce CD8(+) T cells with enhanced lytic activity against neu(+) tumors. PTX treatment also enhances maturation marker expression on CD11c(+) DCs isolated from vaccine-draining lymph nodes. Ex vivo, these DCs activate CD8(+) T cells with greater lytic capability than DC's from vaccine alone-treated neu-N mice. Finally, PTX treatment results in enhanced antigen-specific, IFN-gamma-secreting CD8(+) T cells in vivo. Thus, administration of PTX with a tumor vaccine improves T cell priming through enhanced maturation of DC.
机译：在靶向HER-2 / neu（neu）的粒细胞巨噬细胞集落刺激因子（GM-CSF）分泌全细胞疫苗之前1天给予亚临床剂量的紫杉醇（PTX），可增强neu特异性T细胞反应并减缓neu （+）耐受的HER-2 / neu（neu-N）小鼠的肿瘤生长。我们证明PTX和环磷酰胺（CY）的共同给药可协同减慢肿瘤的生长，并且在LPS成熟之前体外暴露于PTX的DC前体会导致更大的共刺激分子表达，IL-12产生以及诱导具有增强的针对neu（+）肿瘤的裂解活性的CD8（+）T细胞。 PTX处理还增强了从疫苗引流淋巴结分离的CD11c（+）DC上的成熟标记表达。在体外，这些DC激活CD8（+）T细胞的裂解能力比单独疫苗治疗的neu-N小鼠的DC更高。最后，PTX治疗可增强体内抗原特异性，分泌IFN-γ的CD8（+）T细胞的功能。因此，将PTX与肿瘤疫苗一起施用可通过增强DC的成熟来改善T细胞的启动。

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