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首页> 外文期刊>Infection and immunity >Interleukin-12 is critical for induction of nitric oxide-mediated immunosuppression following vaccination of mice with attenuated Salmonella typhimurium.
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Interleukin-12 is critical for induction of nitric oxide-mediated immunosuppression following vaccination of mice with attenuated Salmonella typhimurium.

机译：白细胞介素12对于减毒鼠伤寒沙门氏菌疫苗接种后诱导一氧化氮介导的免疫抑制至关重要。

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Studies from our laboratory have shown that infection of mice with an attenuated strain of Salmonella typhimurium causes a marked suppression in the capacity of splenocytes to generate an in vitro plaque-forming cell (PFC) response to sheep erythrocytes. The suppression has been shown to be mediated by mature, adherent macrophages (Mphis) and nonadherent, precursor Mphis. Nitric oxide has been identified as the suppressor factor. The present study investigated the role of interleukin-12 (IL-12) in the generation of nitric oxide-mediated immunosuppression in this model. Salmonella inoculation resulted in marked suppression of PFC responses and high levels of nitrite production. When mice were treated with anti-IL-12 prior to inoculation, nitrite levels in splenocyte cultures were reduced by 75% and the suppression of PFC responses was prevented. The nonadherent splenocyte fraction from Salmonella-inoculated mice, which contains precursor Mphis and is weakly immunosuppressive, was treated with IL-12 in vitro. IL-12 augmented the capacity of this fraction to suppress PFC responses by normal splenocytes in a coculture system. Additionally, IL-12 induced nitrite and gamma interferon (IFN-gamma) production in a dose-dependent manner. Treatment with anti-IFN-gamma blocked nitrite production and suppression, indicating that IFN-gamma is an important intermediary in the pathway of IL-12-induced immunosuppression. These results indicate that IL-12 is critical for the induction of nitric oxide-mediated immunosuppression following S. typhimurium inoculation and, through its ability to stimulate IFN-gamma production, can induce nitric oxide-producing suppressor Mphis.
机译：我们实验室的研究表明，鼠伤寒沙门氏菌减毒株感染小鼠会显着抑制脾细胞生成对绵羊红细胞的体外噬菌斑形成细胞（PFC）反应的能力。已显示抑制作用是由成熟的粘附巨噬细胞（Mphis）和非粘附的前体Mphis介导的。一氧化氮已被确定为抑制因子。本研究调查了白细胞介素12（IL-12）在该模型中一氧化氮介导的免疫抑制中的作用。接种沙门氏菌可显着抑制PFC响应和高水平的亚硝酸盐生成。当在接种前用抗IL-12治疗小鼠时，脾细胞培养物中的亚硝酸盐水平降低了75％，并防止了PFC反应的抑制。在体外用IL-12处理了来自沙门氏菌接种小鼠的非粘附脾细胞部分，该部分含有前体Mphis，并且免疫抑制性较弱。 IL-12增强了该级分抑制共培养系统中正常脾细胞对PFC应答的能力。另外，IL-12以剂量依赖性方式诱导亚硝酸盐和γ干扰素（IFN-γ）的产生。抗IFN-γ的治疗阻断了亚硝酸盐的产生和抑制，表明IFN-γ是IL-12诱导的免疫抑制途径的重要中介。这些结果表明IL-12对于鼠伤寒沙门氏菌接种后诱导一氧化氮介导的免疫抑制是至关重要的，并且通过其刺激IFN-γ产生的能力，可以诱导产生一氧化氮的抑制子Mphis。

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