To investigate the anti-inflammatory or pleiotropic immunomodulatory role of interleukin-18 (IL-18), collagen-induced arthritis (CIA) mice were administrated with IL-18 along or in combination with IL-10, IL-4 or IL-12. IL-18 treatment along had no therapeutic effect on onset or established CIA mice. However, the combined treatment of low-dose IL-18 with IL-10 ameliorated the disease progression. Th1 cytokine expression was significantly inhibited, whereas Th2 cytokine expression was up-regulated in the synovial tissue by the IL-18/IL-10 treatment when compared with that in control group. Interestingly, IL-18 receptor (IL-18R) alpha expression was down-regulated by the treatment. According to the development of Th2 responses, GATA-3 mRNA expression was significantly increased in the treatment group. Our results indicated that combined treatment of low-dose IL-18 with IL-10 can prevent the development of CIA, which may be mediated not only by inhibiting Th1 responses through IL-18/IL-18Ralpha signaling, but also by inducing anti-inflammatory mediators through a GATA-3-dependent mechanism.

译文

为了研究interleukin-18 (IL-18) 的抗炎或多效性免疫调节作用,将胶原诱导的关节炎 (CIA) 小鼠与IL-10,IL-4或IL-12一起或与之组合给予IL-18。IL-18治疗对发病或已建立的CIA小鼠没有治疗效果。然而,低剂量IL-18与IL-10的联合治疗改善了疾病进展。与对照组相比,IL-18/IL-10治疗在滑膜组织中Th1细胞因子表达被显着抑制,而Th2细胞因子表达在滑膜组织中被上调。有趣的是,IL-18受体 (IL-18R) α 表达被治疗下调。根据Th2反应的发展,治疗组GATA-3 mRNA表达显着增加。我们的结果表明,低剂量IL-18与IL-10的联合治疗可以防止CIA的发展,这不仅可以通过IL-18/IL-18Ralpha信号抑制Th1反应来介导,还可以通过GATA-3-dependent机制诱导抗炎介质来介导。

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