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首页> 外文期刊>Cellular immunology >Cholecystokinin octapeptide significantly suppresses collagen-induced arthritis in mice by inhibiting Th17 polarization primed by dendritic cells.
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Cholecystokinin octapeptide significantly suppresses collagen-induced arthritis in mice by inhibiting Th17 polarization primed by dendritic cells.

机译：八肽胆囊收缩素可通过抑制树突状细胞引发的Th17极化来显着抑制小鼠胶原诱导的关节炎。

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摘要

Cholecystokinin octapeptide (CCK-8) is a neuropeptide, and is shown to be a potent immunomodulator with predominant anti-inflammatory effects. Although the regulatory effect of CCK-8 on macrophages and B cells has been defined, the effect of CCK-8 on dendritic cells (DCs) and T cells is not well understood. In this study, we showed that CCK-8 reduced the expression of CD80, CD86, and MHCII on DCs. Moreover, CCK-8 promoted Th1 and inhibited Th17 polarization by increasing the production of IL-12 and decreasing the production of IL-6 and IL-23 on DCs in vitro and in vivo. In addition, intraperitoneal administration of CCK-8 to mice with collagen-induced arthritis (CIA) was found to effectively reduce the incidence of arthritis, delay its onset and prevent the occurrence of joint damage. Collectively, these results suggest that CCK-8 significantly suppresses the incidence and severity of CIA in mice, through the inhibition of DC mediated Th17 polarization.
机译：胆囊收缩素八肽（CCK-8）是一种神经肽，被证明是一种有效的免疫调节剂，具有主要的抗炎作用。尽管已经定义了CCK-8对巨噬细胞和B细胞的调节作用，但对CCK-8对树突状细胞（DC）和T细胞的作用尚不十分了解。在这项研究中，我们表明CCK-8减少了DC上CD80，CD86和MHCII的表达。此外，CCK-8通过在体外和体内通过增加IL-12的产生并降低IL-6和IL-23的产生来促进Th1并抑制Th17极化。另外，发现对患有胶原诱导的关节炎（CIA）的小鼠腹膜内施用CCK-8可有效减少关节炎的发生，延迟其发作并防止关节损伤的发生。总体而言，这些结果表明，CCK-8通过抑制DC介导的Th17极化来显着抑制CIA在小鼠中的发生和严重程度。

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