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首页> 外文期刊>Cytokine >Principal role of IL-12p40 in the decreased Th1 and Th17 responses driven by dendritic cells of mice lacking IL-12 and IL-18
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Principal role of IL-12p40 in the decreased Th1 and Th17 responses driven by dendritic cells of mice lacking IL-12 and IL-18

机译：IL-12p40在缺乏IL-12和IL-18的小鼠树突状细胞驱动的Th1和Th17应答降低中的主要作用

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摘要

IL-12 and IL-18 are cytokines which are mainly secreted by endothelial cells and monocytes including dendritic cells. The well-known effects of IL-12 and IL-18 in the protection against bacteria and virus infection as well as tumor development are associated with their characteristics in synergistically driving the development of T helper type 1 (Th1) cells and inducing IFN-γ production. In this study, we compared the knockout effects of IL-12 and/or IL-18 genes on phenotypes and functional capabilities of dendritic cells (DCs) including their ability to polarize naive CD4+ T cells. The expression levels of surface molecules such as MHC II, CD80, CD86 and ICOSL, and endocytic capacity were not significantly differences between DCs of wild type (WT) mice and double knockout (DKO) mice of IL-12p40 and IL-18. Additionally, DCs lacking IL-12p40 and/or IL-18 genes were equivalently efficient in inducing T cell proliferation, compared with the WT-DCs. Interestingly, IL-10 production significantly decreased in DKO-DCs, while production of other inflammation-related cytokines were unaffected in WT-DCs and DKO-DCs. Importantly, IL-12p40-/--DCs and DKO-DCs severely impaired the ability to induce IFN-γ and IL-17 production from CD4+ T cells. IL-18-/--DCs also moderately decreased IL-17 production and IL-17-expressing CD4+ T cells when co-cultured with CD4+ T cells, demonstrating the involvement of IL-18 in driving IL-17 differentiation. Taken together, these results suggest the principal contribution of IL-12p40 in inducing Th1 and Th17 polarization, regardless of similar surface phenotypes of DCs.
机译：IL-12和IL-18是主要由内皮细胞和包括树突细胞的单核细胞分泌的细胞因子。 IL-12和IL-18在防御细菌和病毒感染以及肿瘤发展中的众所周知作用与其协同驱动T辅助1型（Th1）细胞发展并诱导IFN-γ的特征有关生产。在这项研究中，我们比较了IL-12和/或IL-18基因对树突状细胞（DC）的表型和功能能力的敲除作用，包括其极化天然CD4 + T细胞的能力。 IL-12p40和IL-18的野生型（WT）小鼠和双敲除（DKO）小鼠的DC之间表面分子（例如MHC II，CD80，CD86和ICOSL）的表达水平和内吞能力没有显着差异。另外，与WT-DC相比，缺乏IL-12p40和/或IL-18基因的DC在诱导T细胞增殖方面同样有效。有趣的是，在DKO-DC中IL-10的产生显着降低，而其他炎症相关细胞因子的产生在WT-DC和DKO-DC中不受影响。重要的是，IL-12p40-/-DC和DKO-DC严重损害了诱导CD4 + T细胞产生IFN-γ和IL-17的能力。当与CD4 + T细胞共培养时，IL-18-/-DCs也可适度降低IL-17的产生和表达IL-17的CD4 + T细胞，这表明IL-18参与了驱动IL-17分化的过程。两者合计，这些结果表明IL-12p40在诱导Th1和Th17极化中的主要作用，与DC的相似表面表型无关。

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