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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Type I IFNs differentially modulate IL-12p70 production by human dendritic cells depending on the maturation status of the cells and counteract IFN-gamma-mediated signaling.
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Type I IFNs differentially modulate IL-12p70 production by human dendritic cells depending on the maturation status of the cells and counteract IFN-gamma-mediated signaling.

机译：I型IFN取决于细胞的成熟状态并抵消IFN-γ介导的信号传导，从而差异性调节人树突状细胞产生IL-12p70。

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摘要

Type I IFNs (IFNalpha/beta) are approved for the treatment of a variety of diseases, including the autoimmune disease multiple sclerosis (MS). The proinflammatory cytokines IL-12 and IFN-gamma have been proposed to contribute to the pathogenesis of MS. Since dendritic cells (DCs) are recognized as major producers of IL-12p70 and promote the development of IFN-gamma-producing Th1 cells, we investigated the direct effect of IFNalpha/beta on monocyte-derived DCs at different stages of development. We demonstrate that IFNalpha/beta enhance IL-12p70 production by immature DCs but inhibit IL-12p70 production by mature DCs. Importantly, IFNalpha/beta strongly counteracted the IL-12-enhancing effect of IFN-gamma on DCs irrespective of their maturation status. Exposure of DCs to IFNalpha/beta during maturation does not affect their maturation or cytokine profile upon CD40 ligation. The differential modulatory effect of IFNalpha/beta on the IL-12-producing capacity of DCs and their cross-regulatory effect on IFN-gamma may reduce inflammatory processes and therefore be therapeutically effective in MS.
机译：I型干扰素（IFNalpha / beta）被批准用于治疗多种疾病，包括自身免疫性疾病多发性硬化症（MS）。已经提出促炎细胞因子IL-12和IFN-γ有助于MS的发病机理。由于树突状细胞（DCs）被公认为IL​​-12p70的主要生产者，并促进产生IFN-γ的Th1细胞的发育，因此我们研究了IFNalpha /β对单核细胞衍生DC在不同发育阶段的直接作用。我们证明，IFNα/β增强未成熟DC产生的IL-12p70，但抑制成熟DC产生的IL-12p70。重要的是，无论其成熟状态如何，IFNα/β都能强烈抵消IFN-γ对DC的IL-12增强作用。 DCs在成熟过程中暴露于IFNalpha / beta不会影响CD40连接后的成熟度或细胞因子谱。 IFNα/β对DCs产生IL-12的能力的不同调节作用及其对IFN-γ的交叉调节作用可以减少炎症过程，因此在MS中具有治疗效果。

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